MedPrepOnline

Principles of Preoperative & Operative Surgery (Part I)

2010-04-22T22:29:00.008+05:00

Preoperative Evaluation-
Aim is not to screen broadly for undiagnosed disease but rather to identify and quantify any comorbidity that may have an impact on the operative outcome. Used to identify risk factors for postoperative morbidity and mortality. Communication between the surgeon and consultants is essential to define realistic goals and to expedite surgical management.

Cardiovascular:
ASA Classification for anesthetic risk has 5 strata:

I- Normal healthy patient
II- Patient with mild systemic disease
III- Patient with severe systemic disease that limits activity but is not incapacitating
IV- Patient who has incapacitating disease that is a constant threat to life
V- Moribund patient not expected to survive 24 hours with or without an operation

Cardiac Risk Indices-
Goldman Cardiac risk Index (1977), Detsky Modified Multifactorial Index (1986), Eagle’s Criteria for Cardiac Risk Assessment (1989), & Revised Cardiac Risk Index.

The current AHA/ACC recommendations are to start Beta-blockers therapy in the medium to high risk patients undergoing major to intermediate risk surgery as early as possible preoperatively and titrate to a heart rate of 60 beats/min.

An easy, inexpensive method to determine cardiopulmonary functional status for noncardiac surgery is the patient’s ability or inability to climb two flights of stairs. Two flights of stairs are needed because it requires greater than 4 metabolic equivalents (METs).

Pulmonary:

Preoperative evaluation of pulmonary function may be necessary for either thoracic or general surgical procedures.

Necessary tests include FEV1, FVC, and the diffusing capacity of carbon monoxide. Adults with an FEV1 of less than 0.8 L/sec, or 30% of predicted, have a high risk for complications and postoperative pulmonary insufficiency.

Preoperative interventions that decrease postoperative pulmonary complications include smoking cessation (>2 months before planned procedure), bronchodilator therapy, antibiotic therapy for preexisting infection, and pretreatment of asthmatic patients with steroids.
Perioperative strategies include the use of epidural anesthesia, vigorous pulmonary toilet and rehabilitation, and continued bronchodilator therapy.

Hepatobiliary:

Evidence of hepatic dysfunction may be seen on physical examination. Jaundice and sclera icterus may be evident with a serum bilirubin level greater than 3 mg/dL. Skin changes include spider angiomas, caput medusa, palmar erythema, and clubbing of the fingertips. Abdominal examination may reveal abdominal distention, evidence of fluid shift, and hepatomegaly. Encephalopathy or asterixis may be evident. Muscle wasting or cachexia can be prominent.

Here are ways to approach a patient with liver disease in selected cases:

Acute Hepatitis-
Postpone elective surgery at least until liver function tests have normalized.

Chronic Hepatitis-
Surgery is generally considered safe in these patients.

Obstructive Jaundice-
1) Perioperative fluid management to prevent renal dysfunction
2) No dopamine or mannitol
3) Lactulose may be helpful
4) Antibiotic prophylaxis
5) No routine preoperative biliary drainage
6) Check for abnormal coagulation parameters

Cirrhosis-
Child’s A and B- Treat ascites, coagulopathy and proceed to surgery
Child’s C- Postpone until the patient’s Child’s class could be improved or cancel surgery for conservative management

Coagulopathy- Target PT to be no more than 2 seconds above normal
1) Vitamin K- 10 mg subcutaneous
2) FFP if no improvement with Vit K
3) Give cryoprecipitate as needed

Ascites-
1) Fluid restriction
2) Diuretics- Furosemide and/or Spironolactone
3) Paracentesis- may be diagnostic or therapeutic with simultaneous administration of albumin

Encephalopathy-
1) Treat with lactulose
2) Prevent by treating precipitating conditions such as GI bleeding, alkalosis, uremia, avoidance of sedatives

Patients with cirrhosis may be assessed with the Child-Pugh classification, which stratifies operative risk according to a score based on several variables. Child’s class A, B, and C have mortality rates of 10%, 31%, and 76% respectfully during abdominal examinations.

Malnutrition is common in cirrhotic patients and is associated with reduction in hepatic glycogen stores and reduced hepatic protein synthesis.

References:
"Sabiston: Textbook of Surgery" Townsend, Elsevier. 2008

More to come soon...

Pediatrics- Ward Notes (Part IV)

2010-04-11T11:37:00.004+05:00

Here are some notes from around the wards during my rotation in pediatrics. Enjoy:

Common causes of Hematuria:
Acute glomerulonephritis, IgA nephropathy, Stones, Urinary tract infection, Clotting disorders, Trauma, Drugs, PSGN

Severe complications of Acute GlomeruloNephritis:
Acute renal failure (anuria), Hypertensive encephalopathy, Left ventricular failure

During the 1st year of life, UTI is more common in males with an M to F ratio of 4:1.
Pyelonephritis characteristically presents with- Fever, Chills, Costovertebral tenderness

Strong indicators of UTI in a Urine D/R: (Multiple organisms usually indicate contamination)
Abnormal color or clarity, > 100,000 of the same organism/ ml, Nitrites +ve, Leukocyte esterase +ve
Damaged RBC casts in urine indicate Glomerular origin.
Creatinine is preferred over BUN because BUN is easily altered by dehydration and starvation while Creatinine is kidney function specific.

-Remember to ask about the number of stools/day because constipation is a risk factor for UTI. Examine the spinal cord.
-When did the child last urinate? If more than 6 hours, then suspect Acute Renal Failure.

Causes of Recurrent UTI:
Hypospadias, Meatal stenosis, Urethral/Ureteric stricture, Renal agenesis, Polycystic kidney disease, Horse-Shoe kidney, Obstruction at the PelvicUreteral Junction, Posterior Urethral Valve

When counseling for urine collection, ask mother if her child informs her when he wants to micturate.

Suprapubic Puncture: Procedure
Bladder should be full (>2 hours since last micturition). Palpate pubic symphysis and then puncture 2-3 cm above in the midline (avascular linea alba). The 10 gauge needle should be perpendicular. Next, aspirate urine out and then seal it. Remember, this is a blind procedure.
Complications- Infection, Trauma, Perforation

Posterior Urethral Valve:
Obstruction at the bladder neck because of posterior mucosal membranes. May present at any age despite being congenital.
Male child, Early presentation, Failure to grow, Oligohydramnios, Anemia, Acidosis, Increase in BP, Big bladder, Palpable kidneys

Investigations- CBC, Urine D/R, UCE, U/S KUB (echogenicity, corticomedullary differentiation, size, diameter, VUR), MCUG, DMSA scan (assess renal function)

Immediate treatment includes bladder decompression via catheterization. Surgical ablation via transurethral approach.

MCUG-
Investigation used for VesicoUreteral Reflux. One should look at the level of dilation of the ureter and the amount of dilation in the calyx and renal pelvis. Normally, contrast should not reflux into the ureters. Posterior urethral valves present as a black band (does not take up dye), between the bladder and urethra.
Urination begins in utero at the 12th week of gestation. Oligohydramnios may result in severe pulmonary hypoplasia. Therefore, a vesicoamniotic shunt should be created.

Ultrasound Kidney:
Echogenicity is compared to the echogenicity of the liver and spleen. The kidneys are normally less.
A dilated pelvis may indicate pelvoureteric stenosis.

DMSA Scan- Used to assess kidney function. A dye is taken up by the renal cortex.
DTPA- glomeruli
MAC 3- Tubules

Causes for Unilateral Kidney damage- Stones, Aberrant vasculature, Ureterocoele, abnormality of the PUJ (can be bilateral)

Grade I or II Hydronephrosis can be treated medically. The patient is advised to 'double micturate'.
Grade IV or V Hydronephrosis is treated surgically. Procedures include reimplantation of the ureters and Deflux surgery.

Management of VUR depends on the degree of damage. The bladder or urethra may need to be completely replaced.

Cesarean section and bottle fed babies are more prone to develop asthma when they grow up.
There is a high association between bronchiolitis and asthma.
A silent chest is a very severe condition.

Chest X-Ray in Asthma patients show streaky hilar shadows, hyperinflation, tubular heart
When Peak Expiratory Flow Rate is graphed, X-axis shows the value while the Height is plotted on the Y-axis.
Honey water or yakhni soup (Pakistani origin) can be given to clear secretions in mild asthma.
Asthma is diagnosed after the 3rd attack.
Status asthmaticus is diagnosed if the 3rd dose of short acting Beta agonists (bronchodilators) does not provide relief. Aminophyllin and steroids should be started.

Eosiniophilia in kids may be seen in:
Asthma, Ascaris infection, Loffler's syndrome, Hay fever, Hookworm infection

Differential Diagnosis for recurrent chest infections:
Cerebral palsy, GERD, Diaphragmatic hernia, DiGeorge’s syndrome, Fungal infection, Heart abnormalities, Pneumonia, Congenital bronchiectasis, Cystic fibrosis, Kartagener’s syndrome

Chest Physiotherapy- Since children under the age of 2 are unable to expectorate, physiotherapy is done to help remove secretions. Lay the child in the lateral tredelenburg position and percuss from below upwards on the chest. This is indicated in Bronchiectasis.

Neonatal Meningitis- E. coli, Group B streptococci, Klebsiella
Infantile Meningitis- H. influenza type B, S. pneumoniae, N. meningitidis
Tubercular Meningitis- glucose levels are low. Choroid Tubercles may be seen in the fundus of the eye
Viral- glucose levels are normal
Herpes- blood may be seen in the CSF
CSF- If there is an increase in lymphocytes, then the origin may be Tubercular, Viral, or partially treated bacterial. Glucose values are the last to change.

A single dose of antibiotics can render a Lumbar Puncture sterile. In such cases, Latex Particle AGglutination should be carried out.
Gram staining, and Herpes PCR can also be performed with CSF along with culture and sensitivity.

Band cells- Are immature neutrophils which signify overwhelming acute bacterial infection. Their nuclear material is arranged in a band within the cell.

Lymphocytic leukocytosis is seen in- Leukemia and Whooping cough

Chloride sweat test (uses pilocarpine) in a suspected Cystic Fibrosis case will be >80 mg/dL.

Barium meals show: Diaphragmatic hernia, Sliding hernia, Achalasia, Esophageal Stenosis/Atresia

Mumps- Advise not to eat sour foods. Complications include meningitis, otitis media, orchitis (males)

Flag sign- Seen in Kwashiorkor. Area of hyperpigmentation alongside an area of depigmentation

Cerebral Palsy- Non-progressive, permanent disorder of posture and movement that is usually a developmental problem. Mental retardation may be associated. Requires multi disciplinary management.

Ampicillin and Gentamycin are given prophylactically to cover gram +ve and gram -ve bacteria.

Dengue antibodies are seen 5 days after the fever begins.

Specific Typhoid investigations- Typhi dot and Bone marrow culture
Cross reactivity amongst Typhoid and Malaria is possible. Previous IgG typhoid is possible with vaccination.
Carriers for typhoid are identified as having three +ve consecutive stool cultures.

Causes of Pancytopenia:
Sepsis, HIV, Megaloblastic anemia, TB, Hypersplenism, Aplastic anemia

Thrombocytosis may be seen in Iron deficiency anemia and Kawasaki's disease.

Causes for Thrombocytopenia:
ITP, Sepsis, Malaria, Hemolytic ureamic syndrome, Hypersplenism, Dengue, TORCH infections, Iatrogenic, DIC, CLD, Hemangioma

Pakistan Statistics-
6 children are born every minute in Pakistan.

Neonatal Mortality rate is 40/1,000 live births, 20 of which are due to birth asphyxia.
Under 5 Mortality rate is 56/1,000 live births.
Perinatal Mortality rate (28 weeks gestation till 7 days after birth) is 60/1,000 live births.
Infant Mortality rate is 91/1,000 live births.
Maternal Mortality Ratio is 276/10,000.

Resuscitation Trolly:
Ambu bag (30-40 mm Hg pressure in infant type), Heater, ET tube (2.5 - 7.0), Laryngoscope, Mouthpiece, Epinephrine, Vitamin K, I/V chamber.

Incubators are used to regulate ventilation and temperature at 37 C degrees.
Blue light is usually used for phototherapy but cyanosis may not be seen. Hence, a yellow light may be used.

Babies at risk for Hypoglycemia- Birth asphyxia, Prematurity, Infants of Diabetic Mothers

If a neonate is limp, apply a painful stimuli. Start CPR when HR <>

Indomethacin is given for a duration of 3 days only after platelet and creatinine levels are termed normal.
Survanta- 4 mL/kG via endotracheal tube.

APGAR score of >7 is considered good.

As this is a series, there will be more to come soon!

Pediatrics- Ward Notes (Part III)

2010-04-03T22:52:00.003+05:00

Here are some notes from around the wards during my rotation in pediatrics. Enjoy:

Hemolytic Uremic Syndrome:
Decreased platelets, Anemia, Peripheral film shows egg shaped cells/burr cells

Congenital Adrenal Hyperplasia:
21 alpha hydroxylase deficiencies are the most common. It causes virulization in females of feminization in males. Cortisol is not formed. Males are usually dehydrated. Urinary 17 ketoesterides is diagnostic. 17 hydroxyprogesterone levels in blood can be checked as well.

Global Retardation- Considered when all developmental parameters are deficient. Chronic Severe Malnutrition- Considered when all 3 growth parameters are <>

Complications of multiple blood transfusions:
Hemosidereosis, Blood group incompatibility, Splenomegaly
Treatment- Deferoxamine

Pneumonia:
Investigations- CBC, CXR, ABG’s (hypoxia, metabolic acidosis, hypercapnea), UCE, Blood culture, Tracheal swab/Bronchial lavage Immediate management- Oxygen, Electrolytes, Antibiotics
Pneumonia should be treated with antibiotics for 5-7 days. Identification of lobe involved can be checked by percussing laterally.
Atypical viral respiratory infections and Sarcoidosis can mimick Miliary TB in a CXR.

Causes of Microcephaly:
Trisomies, TORCH infections, CHARGE syndrome, Cruzen syndrome (early fusion of skull bones)

D/D for 1 day high grade fever with Neutrophilia- Bacterial tonsillitis, Pharyngitis, Otitis media, Urinary Tract Infection

Guillan Barre Syndrome is a lower motor neuron lesion.

Causes for a false -ve Monteux test- Steroid drugs (>20 mg/day for 2 weeks), Grade III malnutrition, Active measles infection

Rickets (Vitamin D deficiency in children):
Repeated chest infections, Craniotabes (ping pong head), Caput quadratum (square shaped head), Wide fontanelle, Frontal bossing (also seen in thalassemia), Pot belly, Widening of wrist, Harrison's sulcus, Rachitic rosary

In the history, ask about adequate sun exposure (UV rays do not penetrate household glass windows), ask about drinking cow's milk (high phosphate content in cow's milk binds to calcium and causes excretion).

Measles:
Fever, Maculopapular rash (appears at the hairline and behind the ears, extends downwards across the whole body, and then disappears in the same fashion of appearance), Cough, Coryza, Conjunctivitis, Koplik spots (white/sandy color spots found in the buccal mucosa in front of the lower molars. These appear before other symptoms). When the rash for Measles subsides, it leaves a dark, desquamated appearance. Measles antibodies may be seen 4-28 days after the rash appears. Ask about vaccination and drug history/allergies.

D/D Measles- Rubella, Scarlet fever, Meningococcemia, Typhoid (rose spots), Insect bites, Drug rash Measles is associated with a high grade fever while Rubella's fever is low grade with enlargement of the posterior auricular and occipital lymph nodes.
Scarlet fever has a dry, sand paper rash present on the upper limbs and trunk and is seen usually at 5-15 years of age.
Meningococcemia presents with meningeal irritation, petechial hemorrhage, and urological symptoms.

Complications of measles: Pneumonia, Laryngitis, Meningitis, Encephalitis, Otitis media, Diarrhea, Myocarditis, Encephalitis, Reactivation of primary Tuberculosis

Measles encephalitis is of 3 types: Measles encephalitis (viremia), Post measles encephalitis (autoimmune), Sub Sclerosing PanEncephalitis (may occur years later)

Measles treatment: Keep the patient at home, Antipyretics, Cough suppression, Nutrition (fluids and diet in short intervals), Antibiotics for superimposed infections.
Vitamin A should be given orally in all children with measles. 100,000 IU in children <>1 year.

Measles surveillance in Pakistan- Serology (2 cc) of patients with clinically diagnosed cases of measles are sent to Islamabad.

Daily requirement of Vitamin A is 1,500 IU. Vitamin A is not available over the counter in Pakistan. Thus, the multivitamin Rovigon (30,000 IU) is given instead.

Vit A deficiency- Night blindness, Xerosis conjunctiva, Xerosis cornea, Thisis bulba

Short Stature:
If systemic causes, then patient is short and thin. If endocrinological causes, then patient is short and obese. Height velocity is important.

Factors effecting growth in utero- Uterine size, Nutrition, Insulin, Insulin like growth factors.
Growth hormone and Thyroid hormone play a vital role in the post natal growth process.
Children whose absolute height is below 2 SD from the mean have pathological growth abnormalities.
Observe the child’s height over a period of at least 6 months. Precocious puberty can cause early bone fusion and a deranged bone age.

Target Height- Determines genetic growth potential. Calculate Mid-Parental height as well. Arm span may also be used if unable to obtain a standing height.

Short stature should be determined as proportionate or disproportionate.
Upper segment : Lower segment ratio- 1.7 at birth, 1.3 at 3 months, 1 at 10 years.
Skeletal dysplasias (spondylodysplasia) and Klinefelter’s syndrome are associated with a decreased U:L ratio. Achondroplasia is associated with an increased U:L ratio.

Proportionate with Increased Ht/Wt- Growth hormone deficiency, Hypothyroidism
Proportionate with Decreased Ht/Wt- Malnutrition, Renal disease, Chronic diseases/infections.

Normal variants of short stature include- Familial short stature and Constitutional growth delay.

As this is a series, there will be more to come soon!

Pediatrics- Ward Notes (Part II)

2010-03-25T20:37:00.002+05:00

Here are some notes from around the wards during my rotation in pediatrics. Enjoy:

Metabolic Profile Investigations:
ABG's, Urinary amino acid chromatography, Sugar chromatography, Serum ammonium levels

Subtle Seizures- lip smacking, cycling movements, repetitive swallowing. 50% of neonatal seizures are subtle.
Jitteriness is differentiated from seizures by physically holding the child's hands. If the movements stop, then it is considered to be Jitteriness. If the movements cannot be forced to stop, then it is a Seizure.
Jitteriness may be caused by hypocalcaemia or hypoglycemia.

ER management of Neonatal Seizures:
Establish and maintain Airway Breathing Circulation, I/V Dextrose for hypoglycemia, I/V calcium for hypocalcaemia, Drugs
Uncontrolled seizures may be controlled with- Paraldehyde (suppository), Pyridoxine (vitamin B6), Generalized anesthesia

Drugs for seizures should not be discontinued unless there is a 2 year seizure free interval.
Teachers usually pick up Petit Mal seizures. Thus, counseling is necessary.

Risk factors for simple febrile fits developing into Epilepsy: (bad prognostic signs)
Young age of onset, Abnormal development, Delayed milestones, Prolonged duration of fits, Increased frequency of fits, Family history of seizures.
There is a 10% chance that complex seizures will develop into Epilepsy.

Before making the diagnosis of Febrile Fits, make sure you check for the signs of underlying Meningitis and Encephalitis:
Meningitis- Bulging anterior fontanelle (this may be the only sign present in a 6 month old child), Brudzinski's sign +ve (involuntary flexion of the legs when the neck is placed in flexion), Kernig's sign +ve (flexion of the leg 90 degrees at the hip joint with pain on extension of the leg thereafter)
Encephalitis- Drowsiness, Increased tone, Babinski's sign +ve (fanning out of the toes with extension of the halux when a painful stimulus is applied)

Infantile spasm- West syndrome. “Salaam” posture. Flexion.

Side Effects:
Phenobarbitone- Irritability, Behavioral changes, Ataxia, Exfoliative dermatitis
Phenytoin- Gingival hyperplasia, Hepatotoxicity, Folate deficiency, Ricket's, Hypersensitivity, Steven Johnson syndrome
Tetracycline- discoloration of teeth
Co-Trimoxazole- Steven Johnson syndrome, bone marrow suppression
Chloramphenicol- aplastic anemia, bone marrow suppression, grey baby syndrome
Cyclophosphamide- Infertility, Alopecia, Bone marrow suppression, Hemorrhagic cystitis

D/D's for fits with CNS infection:
Meningitis, Encephalitis, Cerebral malaria, Tuberculosis, Otitis media, Brain abscess (focal lesion)

D/D's for Focal seizures without Fever:
Stroke, Thrombus, Cardiac defects (endocarditis, PDA, arrhythmias), Hypocalcaemia, Autoimmune, Coagulopathies, Dehydration (causes hyperviscosity and stasis of blood), Polycythemia

SIADH may lead to seizures via hyponatremia.

Diarrhea:
Chronic Diarrhea- Diarrhea for 2 weeks with no organism detected. Diarrhea is defined to be 2-3 episodes of loose watery stools more than usual.
Safe water- Water suitable for drinking that is free of bacteria/contaminants and has normal biochemical values.

Indications for antibiotics in acute watery diarrhea:
Blood in stool, Suspected cholera outbreak, Amebiasis, Giardiasis, Focus of infection is outside of the GIT

Risk Groups for Dehydration:
Children <1>5 diarrheal stools within the previous 24 hours, Malnutrition, Children who cannot tolerate ORS before presentation, Infants who stop breastfeeding during illness.

Complications of Diarrhea:
Dehydration, Hypovoluemic shock, Metabolic acidosis (bicarbonate in stool), Renal failure, Hypokalemia, Hyponatremia (seizures), Hypoglycemia, DIC, Aspiration pneumonia
Signs of Hypokalemia- Paralytic Ileus (post diarrheal dehydration), Muscle weakness, Arrhythmia, Sluggishness

Treat dehydration with Ringer's lactate 100 mL/kg/day.
For ongoing losses use 1/5th Dextrose saline 250 mL/kg/day.
Potassium is supplemented over a time frame of at least 6 hours. Otherwise, cerebral edema may occur.
Normal saline can be used to compensate for losses of Vomiting.
Daily Na+ requirement is 2-3 meq/kg.
Ringer’s lactate does not cause sodium excess. It expands the circulating volume and helps correct metabolic acidosis. Ringolactate D has the addition of 5% dextrose.

Metabolic acidosis causes a shift in Potassium ions. 40 mEQ is the maximum amount of Potassium put in I liter.
The addition of exogenous potassium causes a “layering effect” because potassium floats to the top of the solution. Potassium chloride is notorious for this effect. This is avoided by using Plabolyte, a homogenized solution in which every drop has the same solution.

Diarrhea presents with deep, rapid breathing. To collect a stool sample, ask the mother to flip the diaper inside out.
Post diarrheal distention is mainly Iatrogenic. Causes include unnecessary antibiotics in viral causes, and use of anti-motility drugs.
New ORS has an osmolarity of 245. Glucose 75, Sodium 75.

Hypernatremic Dehydration: Suspected when mothers incorrectly prepare ORS or powdered milk formulas. Present with Jittery movements, Increased muscle tone, Hyperreflexia, Convulsions, Coma.

KYB diet- Kichiri, Yogurt, Banana.

Pulsus Alternans- Left ventricular failure

Pulsus Paradoxus:
Cardiac- Pericardial effusion, Cardiac tamponade, Cardiogenic shock
Pulmonary- Pulmonary embolism, Asthma, COPD
Others- Superior vena caval obstruction, Anaphylactic shock

Waterhammer (collapsing) Pulse:
Physiologic- Fever, Pregnancy
Cardiac- Hypertension, Bradycardia, Aortic regurgitation, PDA
Others- Anemia, A/V fistula, Beri-beri deficiency, Cirrhosis, Cor pulmonale, Thyrotoxicosis
(Mnemonic for Others- AABCCT)

As this is a series, there will be more to come soon!

Pediatrics- Ward Notes Series (Part I)

2010-03-18T21:01:00.003+05:00

Here are some notes from around the wards during my rotation in pediatrics. Enjoy:

Schedule for vaccinations outside of EPI:
Previnar (Pneumococcal vaccine against S. pneumoniae)- 2nd, 4th, and 6th months
Rota Virus (Diarrhea)- 2nd and 4th month. Contraindicated after 6 months of age because of high risk of Intussusceptions
MMR (Measles, Mumps, Rubella)- 15 months, 5 years, and 10 years
Varicella (Chicken Pox)- 1st and 2nd years
Typhoid (Dysentery)- 2 years, then repeat every 3 years
Flu Shot- Normally given in the winter season, especially in children with Asthma, Cystic fibrosis, or Heart disease
Hepatitis A- Two doses, 6 months apart
Meningococcal (Meningitis)- Given to those children with a history of recent contact, family history, Hajj pilgrims, dormitory students, and army soldiers
HPV (Cervical cancer)- HPV strains 6, 11, 16, 18 are most common. Two doses are given beginning at the age of 9 years

Contraindications for Pertussis vaccine- Anaphylaxis or Encephalitis within 7 days of previous injection.
DTaP- for acellular pertussis. Contains different antigens from DTP.
Generally, Polysaccharide vaccines are not effective before the age of 2 years.

General Physical Examination:
Introduction, Ask permission, Record height and weight and note percentiles, Record vitals (BP important in GBS because of autonomic innervation), Comment on nutritional status, Look for scars, Signs of Jaundice, Conjunctival anemia, Periorbital edema, Nails, Ears, Buccal mucosa, Clubbing, Palms, Pedal edema (non pitting edema found in Myxedema-thyroid).
Extent of Edema is checked by ascending from the feet upwards. Abdominal wall edema is checked by pinching laterally (like skin pinch). Scrotal edema is checked by having the patient sit up for support (edema may be caused by infections).

Liver Palpation- Tenderness, Size, Span, Consistency, Margins, Surface, Bruit
Liver size is measured in centimeters palpable below the coastal margin, midclavicular line. When the liver is not palpable, there is no liver size.

Describing a Rash:
Site, Onset, Character, Itching, Color, Fever, Etiology

CardioVascular Examination:
Comment on the location and character of the Apex beat. Palpate for thrills in all areas.
Character- Tapping (RVH), Hyperdynamic (LVH), Forceful
Left parasternal heave is seen in Right ventricular hypertrophy.
Apex beat heave is seen in Left ventricular hypertrophy.

Murmurs:
Pulmonary Stenosis murmur- Harsh, systolic murmur. Radiates to the neck.
ASD murmur- Blood volume overload causes a Harsh, ejection systolic murmur.
VSD murmur- Harsh, pansystolic murmur. S1 is normal. If there is an associated loud P2, then there is also Pulmonary Hypertension.
Mitral Regurgitation murmur- Pansystolic murmur at the apex beat, radiating to the axilla. S1 is soft.

Clinical signs of Heart Failure:
Edema, Tachycardia, Basal crepts, Hepatomegaly, Galloping heart (S1+S2+S3)

How to differentiate the Spleen from the Kidney on examination:
Spleen moves on inspiration, the Upper border of the spleen cannot be palpated, Splenic notch will be felt on palpation of spleen while the normal round contours of the kidney will be felt otherwise, Spleen lays directed obliquely towards the right iliac fossa, Spleen cannot be palpated bimanually, Spleen has a dull percussion note while since the Kidney lays retroperitoneal there is no percussion note because of overlaying colon

Liver Function Tests:
If the major component of total bilirubin is Direct, then the cause is either Hepatic or Post Hepatic.
If the major component of total bilirubin is Indirect, then the cause is Hemolytic.
If Gamma GT is increased, then the cause is Obstructive.

Weight is an assessment of current nutrition while Height is an assessment of previous nutrition.

Two signs of BCG vaccination- Scar and Mantoux conversion

CT findings in Meningitis- Hydrocephalus, Meningeal enhancement, Periventricular darkening

Anterior fontanelle should close within the 8th to 18th months.
1 oz of milk (30 ml) has 23 calories.

Pinpoint pupil- Horner's syndrome, Morphine intoxication, Hypothalamic lesion
Mid-dilated pupil- Lesion in the Midbrain or Pontine

Papilledema is seen in raised intracranial pressure states.

Nasogastric Tube:
Indications- Diagnostic (stomach pH, stomach pressure), Therapeutic (gastric decompression, intestinal obstruction, esophageal varicies, paralysis of the muscles of mastication)
Contraindications- Esophageal tumors. Nasal polyps, Tonsillitis, Trauma to face
Complications- Trauma, Insertion into the trachea, Perforation, Kinking, Damage to nasal mucosa

Pulse in Anemia- Hemodilution causes rapid, strong, bounding pulse.
Pulse in severe Dehydration- Rapid, low volume, feeble pulse. There is associated decreased urinary output, cold extremities.

Waterhammer Pulse:
AV malformation, Thyrotoxicosis, PDA, Aortic regurgitation

Birth weight should be 2.5-3.5 kg. This is normally doubled at 5 months, tripled at 1 year, and quadrupled at 4 years.
Pulse of a full term newborn should be 120-160 beats/min.
Respiratory Rate of a full tern newborn should be 40-60 breaths/min.
Large babies (macrosomia) are at risk for- Hypoglycemia (glucose < 40), Hypocalcaemia, Cardiac lesions, Respiratory distress syndrome

Primitive reflexes include:
Sucking, Rooting, Grasping, Plantar, Moro's, and many others

X-Ray Skull:
Periventricular calcification- Cytomegalo Virus infection
Diffuse calcification- Toxoplasmosis infection
Premature babies are more prone to Intraventricular Hemorrhage

Thymic shadow normally persists up until the age of 6 months.

Points to note when taking a History of an Anemic patient:
Nutrition, PICA, Worms, Chronic infections, Lead poisoning, Rectal polyps, Prematurity, Twin-twin Transfusion syndrome, Feto-Maternal Transfusion syndrome, Hemorrhage, Hemolytic disease of newborn

Sites to check for Anemia:
Bulbar conjunctiva, Palms (darkened creases & redness), Nails, Buccal mucosa, Soles of feet

Risk factors for Anemia in Breastfed children:
Iron deficiency in Mother, Low birth weight, Late weaning

Diseases causing Anemia of Chronic origin (normocytic, normochromic)- Tuberculosis, Chronic liver disease, Chronic renal disease, Cystic fibrosis

Anemia workup- Reticulocyte count, Iron profile, Peripheral smear, Electrophoresis

Bone marrow profile with Iron staining is the gold standard to investigate for Iron deficiency anemia.
M:E ratio- Myelo Erythropoietin ratio??
6 mg/kg/day of iron in ferric form with meals should be given for 3 months to correct anemia.

Causes for Anemia with hepatosplenomegaly:
Thalassemia, Malaria, Sickle cell anemia, Leukemia, Hereditary spherocytosis, Autoimmune hemolytic (SLE, Drugs), Hypersplenism, G6PD deficiency, Portal hypertension/CLD, Glycogen storage disorders, TB, Ventricular heart failure
Investigations- CBC, Peripheral smear, Blast cells, Electrophoresis, Bone marrow scan, Solubility, G6PD levels.
Treatment- According to cause. Bone marrow transplant. Transfusion every 3-4 weeks lifelong with a chelating agent to avoid iron overload.
Complications- Infections (Hepatitis B & C), Malaria, Dengue, Heart failure, Congestive cardiac failure, Hemodermatosis, Growth retardation, Hypersplenism, Growth hormone deficiency, Hypothyroidism
Prevention- Avoid consanguineous marriages, Chorionic villous sampling before 12 weeks for abortion, Amniocentesis

Pallor becomes evident when hemoglobin levels are less than 7 g/dl.
HbF peaks at 26-28 weeks and persists until 6 months of age.
Serum ferritin may be increased simply due to fever.
The first indicator of appropriate iron therapy is Reticulocyte count. Clinically, cognitive functions will be the first to improve.

As this is a series, there will be more to come soon!

Migraine

2010-02-24T20:40:00.004+05:00

Migraine is recurrent headache associated with visual and GI disturbance. Approximately 12% of the population world-wide suffers from the condition.

Pathology:

Precise mechanisms are still unknown. Although some factors are as follows:

1) Genetic factors play some part;
2) Also, release of neuropeptide, calcitonin-gene-related peptide (CGRP) is implicated as it is a potent dilator of cerebral and dural vessels.
The headache of migraine is usually caused by dilation or edema of cranial vessels and subsequent stimulation of nearby nerve endings. Nitric oxide, a vasoactive substance, also has a role. Magnesium deficiency, nueral excitation by glutamate and asparate as well as alterations in hypothalamic-pituitary axis is also suggested.

Some precipitating factors:
1) Weekend migraine (time of relaxation)
2) Chocolate (phenyl ethylamine)
3) Cheese (high in tyramine)
4) Noise and irritating lights
5) Premenstrual symptoms
6) Also common around puberty and menopause

Clinical Presentation:

1) Migraine with aura - prodromal symptoms are usually visual mostly related to visual cortex depression or retinal problems. Other neurological symptoms like tingling, nausea, numbness and vague weakness of one side may occur. It can last for few minutes to an hour followed by the headache. It is usually hemi cranial but often begins locally. Patient is irritable and prefers dark environment. Diuresis follows resolution after several hours and deep sleep often ensues.

2) Migraine without aura (common migraine) - the usual variety. Prodromal symptoms are vague and headache is recurrent accompanied by nausea and malaise.

3) Basilar migraine - prodrome includes vertigo, diplopia, transient visual disturbance, syncope and dysarthria. They can occur alone or progress to typical migraine

4) Hemi paretic migraine - classical migraine with hemi paretic features, but resolves within 24 hours differentiating from stroke.

5) Ophthalmoplegic migraine - associated with third nerve, or sometimes sixth nerve palsy.

6) Facioplegic migraine - associated with unilateral facial palsy.

Differential Diagnosis:

The sudden headache may resemble meningitis or Sub-Arachnoid Hemorrhage. Prodromal symptoms must be distinguished from Transient Ischemic Attacks - TIAs usually deficit immediate and without headache.
Sensory abnormalities may resemble sensory epilepsy.

MANAGEMENT:

General measures include:
1) Reassurance and relief of anxiety
2) Avoidance of dietary factors - rarely helpful. Also patients taking oral contraceptives may benefit from change of brand or trying without. Severe symptoms are indication for stopping hormonal medications.

During an attack:
After ruling out serious pathology for headache, paracetamol or other simple analgesics should be given, with an antiemetic (e.g. Metaclopromide) if necessary. Repeated use may lead to further headaches.
Also, Triptans (5-HT1 agonists) can be used as well. In 30% cases of severe recurrent migraine, sumatriptan, zolmitriptan and naratriptan are of value by either subcutaneous injection or orally by inhaler. They should be avoided when there is vascular disease. Recently, some CGRP antagonist was effective in treating attacks.

Prophylaxis:
The following are used when attacks are frequent:

1) Pizotifen (antihistamine and 5-HT antagonist) - 0.5mg at night for several days, increasing to 1.5mg (common side-effects: weight gain and drowsiness)
2) Propanolol (beta-blocker) - 10mg three times daily, increasing to 40-80mg thrice daily
3) Amitriptyline - 10mg (or more if required) at night

Sodium valproate, methysergide, SSRIs, verapamil, topiramate and nifedipine are also used.

Hopefully the article would help my fellow medical students understand migraine better for it is a common problem encountered by most GPs and even by us students during daily life.

(Sources: Kumar and Clark, Davidson)

Pulmonary Edema

2010-02-15T00:11:00.005+05:00

PULMONARY EDEMA
Fluid accumulation in lungs, causing impaired gaseous exchange leading to respiratory difficulty/ failure.

TYPES:
Cardiogenic
Non-cardiogenic

CLINICAL FEATURES:
Dyspnea
Cough
Pink frothy sputum
Restlessness
Excessive sweating

In chronic cases, there maybe:

Nocturia
Pedal edema
Orthopnea
Paroxysmal nocturnal dyspnea

MANAGEMENT OF ACUTE PULMONARY EDEMA

Diagnosis:

Clinical Signs:
Decreased peripheral perfusion
Pulmonary congestion
Use of accessory respiratory muscles
Wheezing, specially in basal zones
Pink frothy sputum

Radiographic Signs: on CXR:
Cardiomegaly
Vascular engorgement (interstitial and perihilar)
Kerley B lines
Pleural effusion (varies with severity)

Treatment:
Start on clinical judgement only, no time to waste.

Position: Nurse the patient in a propped up position, so the secretions don’t pool in the bases of lungs.
Relieving the dyspnea: Administer oxygen, so arterial pO2 comes up to 60%.
Administer IV furosemide (loop diuretic), which actys as a venodilator before its diuretic action comes into play, thus immediately relieves edema. Nitroglycerin potentiates the effects of loop diuretic, so it is usually also given. Mechanical ventilation is indicated if hypercapnea coexists.
Relieving the pain: Provide analgesia(morphine sulfate) if patient experiences any pain, as pain may exacerbate the dyspneic symptoms.
Supportive: Inotropic agents are indicated if patient is in cardiac block or shock, eg. dobutamine or PDE inhibitors.
Recombinant BNP: Nesiritide, indirectly increases cardiac output. It also produces diuresis and natriuresis, in conjunction with furosemide.
Acute hemodialysis and ultrafiltration: consider in patient with significantly renal dysfunction and diuretic resistance.
Heart catheterization
Correction of precipitating factors: HTN, MI, ischemia, acute valvular regurgitation, arrhythmias or volume overload should be corrected for.

Alzheimer's Disease - Dementia

2010-02-07T00:34:00.008+05:00

What is Dementia?

An acquired global impairment of personality, intellect and memory without any impairment in consciousness.

Dementia can either be progressive or non progressive depending upon the cause. It is noteworthy that Dementia is NOT a disease, it is simply a collective name given to a a group of disorders that may bring about the changes in memory, intellect and personality.

ALZHEIMER'S DISEASE

A TYPICAL CASE SCENARIO of Alzheimer's Disease:

"A woman in her early 50s was admitted to a hospital because of
increasingly odd behavior. Her family reported that she had been
showing memory problems and strong feelings of jealousy. She also
had become disoriented at home and was hiding objects. During a
doctor's examination, the woman was unable to remember her
husband's name, the year, or how long she had been at the hospital.
She could read but did not seem to understand what she read, and
she stressed the words in an unusual way. She sometimes became
agitated and seemed to have hallucinations and irrational fears."

Alzheimer's Disease is the leading cause of Dementia amongst the older people today.

According to the latest epidemiological survey, this progressively detoriating cause of dementia effects about four million people in the United States of America. 1 in every 10 people will suffer from Alzheimer's disease in the population of people greater than 65 years of age. This figure, however, becomes a staggering 1 in ever 2 persons for people over the age of 85 years. Approximately, fifty thousand deaths in the USA are directly caused by Alzheimer's disease. So yes, you are dealing with a big problem!

What causes Alzheimer's Disease?

Extensive research has been targetted at finding the basic cause of the development of this progressive dementia however, no single factor can yet be labelled as the soitary cause of Alzhiemer's Disease. Many pathology causing theories have been put forward amongst which the most widely accepted conclude the presence of :

*Neurofibrillary tangles in the Cortex of the Brain
*Amyloid or Senile Plaques
*Widespread loss of Acetylcholine in the CNS
*Selective neuron loss in the Hippocampus and Entorhinal areas the brain
*Decrease in the number of synapses in the CNS
*Tau protein abnormalities

Signs and Symptoms

The presence of signs and symptoms, in the early stages of the disease, are very much dependant on the pre-morbid personality of the individual. A shy, reserved and introvert type of a person will show more signs of the disease at an early stage whilst a socially skilled person can go on functioning adequately till much later stages of the disease.

*Memory Impairment --> This is the foremost sign of AD. Initially the short term memory is effected. The patients will have trouble understanding new concepts or new routines. They will forget their new neughbour's name however will not forget how to ride a bicycle, in the initial AD stages. In later stages the long term memory is also hampered.

*Mood Disturbances/Behavioural Changes --> Fluctations in the moods are present varying from depression to anger to aggressive behaviour. Many patients lose their social inhibitions and commit various embarassing actions like undressing in public etc.

*Catastrophic Reactions --> Patients, when moved from routine, can show signs of aggression

*Organic Orderliness --> A patient of Alzheimer's Disease likes to live by a very strict routine.

*Psychotic Symptoms --> Some of the patients may harbour Depression while some have been reported to have haluucinations. The most common Hallucinations known to occur in an Alzheimer's patient are Persecutory Hallucinations (patients complain of theft or robbery when nothing has happened in actuality).

Risk Factors

Genetics and Family History

Advancing Age

Smoking

Alcohol

Atherosclerosis

Increases plasma Homocysteine levels

Diabetes Mellitus

Down's Syndrome

Mild Congnitive Impairment (MCI) ---> One study claims that 40 percent of over 65 years inviduals who had MCI developed Alzheimer's Disease within the next three years!

Diagnosing Criteria

Comprehensive History and Examination to rule out any other problems
Mini Mental State Exam
MRI
EEG

According to DSM IV, the presence of the following features is necessary to label a person suffering from Alzheimer's Disease:
*Memory Impairment

*One or more of --> Aphasia,
Apraxia,
Agnosia,
Disturbance in Executive Functioning

*Exclusion of other organic disorders

Treating Alzheimer's Disease
Though there is no cure for Alzheimer's, the treatment aims to increase the quality of the life of the patients. A BioPsychoSocial standard plan for the treatment of Alzheimer's disease is given below.

Bio or Medical Therapy: Though there are devised medications for the treatment of Alzheimer's disease, it is important to remember that this a disease that runs on a one way road only, there is NO cure for Alzheimer's as yet. Medications will help the symptoms of the disease to get better but it cannot slow down or cure the disease.

*Choline esterase inhibitors (Tacrine, Donezapil, Rivastigmine, Galantimine) are the mainstray therapy. They work to increase the amount of Acetylcholine in the CNS, as these patients have increasingly low levels of AcH in their systems.

The following are given to the patients with specific symptoms:
*Anti Convulsants
*Sedatives
*Anti Depressants

Psychosocial Help
Secure Environment and Understanding:
The patients of Alzheimer's Disease require continous care by the ones looking after them. They need understanding and love. A normal routine life in a loving and caring environment is perhaps the answer to alot of poblems they face. These patients should be kept away from harm's way. All harmful objects in a household should be kept locked away from their way and they should not be allowed to drive themselves or go wandering about by themselves.
Care takers might feel burdened by the round the clock care needed by their loved ones suffering from Alzheimer's so it is necessary to take timely shifts in doing the duty.

Cognitive Therapy, Leisure activities and Exercise should be encouraged amongst these patients.
Support Groups help can seeked as needed.

Thyroid Examination

2010-02-06T06:33:00.004+05:00

Thyroid Examination

Greet the patient -> handshake
- Handshake
  1. Sweating
  2. Normal temperature
  3. Pulse?
Explain
Seek permission
Right side always
Proper exposure
Ensure privacy

General Inspection:

Appropriately dressed for temperature outside?
Comment on obesity, weight loss
Anxious, agitated, lethargic?
Exophthalmos
Dry skin (hypothyroidism)
Hair – loss?
Facial myxedema?

Examination of the hands:

Check pulse (bradycardia, tachycardia, atrial fibrillation)
Check for presence of sweating, increase in temperature, palmar erythema?
Onycholysis (separation of the nail from its bed)
Thyroid acropathy (similar to clubbing)
Ask the patient to extend arms and hold hands with palms facing downwards. Check for fine tremors.
- Rest piece of paper over hands
Elicit Pemberton's sign
- It is the development of facial flushing, distended neck and head superficial veins, inspiratory stridor and elevation of the jugular venous pressure (JVP) upon raising of the patient's both arms above his/her head simultaneously, as high as possible.

Examination of the thyroid gland:

Inspection:

Comment on symmetry, scars
Obvious thyroid enlargement?
Midline masses?
Ask the patient to swallow (only goiter or thyroglossal cyst rises upon swallowing)
Protrude the tongue (thyroglossal cyst moves with protrusion of tongue)
Comment on the mass
- The 7 S's (BOX)
- Distention
- Discharge
- Extension

Inspection 7 S's

Site (anterior triangle)
Size (3x3 cm)
Shape (spherical, uniformly enlarged or nodular)
Surface (smooth, rubbery, hard)
Surrounding skin (normal, ulcers, sinuses)
Scars (none)
Subcutaneous veins (not)

Palpation:

Stand behind the patient
Thumbs on back of neck, patient's head slightly flexed
Palpate neck
Ask to swallow and feel the gland move under your fingers (Get below the swelling)
Palpate right lobe
- Turn neck slightly to right
- Ask to swallow
- If palpable, describe size, shape, consistency, tenderness, mobility
  - Temperature à surrounding and then on lump
  - Tenderness
  - Texture
  - Trachea
- Repeat for left lobe!
Lymph nodes palpation; also check Virchow's glands

Percussion:

From down upwards; check for retrosternal extension
Also percuss clavicle

Auscultation:

Bruit is a sign of increased blood flow; maybe present in thyrotoxicosis
- Take breath in and hold while auscultating
- Auscultate over two major lobes
- Auscultate with bell
  - Also auscultate mitral area

Examination of the eyes:

Lid lag, lid retraction
Chemosis, Proptosis
Exophthalmos (examine from above & behind, from side. Eyes should not be visible beyond the supraorbital ridge)
Check eye movements (ophthalmoplegia); seeing double?

Miscellaneous:

Check reflexes
Proximal myopathy
Pretibial myxedema
CVS examination (failure?)
Internal carotid

BBBRRRRIIIINNNNNGGGGG!!!!

2010-01-20T20:05:00.005+05:00

6:00 AM
Wake up alarm goes off.

6:45 AM
Ten snooze buttons later…. the time you really wake up. You wash your face and brush your teeth. Quickly iron your clothes and then jump in the shower. Chomp down breakfast while reviewing some notes for the upcoming day.

7:30 AM
You make that breakfast “to go” by throwing the last huge bite in your mouth and run out the door. WAIT… STOP!! Quick u-turn, run up to your room to grab your white coat, and now you can hussle your way out the door and into your car. Off to the hospital.

8:00 AM
You’re honking your horn like a madman on the road. Don’t these people know I have patients to write SOAP notes on before the consultants get there for grand rounds!?!?!!

8:45 AM
After frantically fidgeting through patient files, and with a little help from the residents, Dr. XYZ gives you the OK. You’re clear. Phew, that was close! Time to relax a bit in the seminar on patient ethics in 5 minutes.

10:00 AM
Off to the wards to check up on patients… this time thoroughly. Make sure you greet the nurses, after all, they are a med students best friend.

1:00 PM
Lunch break and preparation for case presentations in the afternoon. Remember to SIT DOWN and take a load off those feet. Your gunna be on them again for the next 4 hours, minimum.

4:00 PM
Hit the library. If you’re lucky, you can get a couple of hours of some solid textbook studying in.

6:30 PM
Clinics and OPD. You better hope these patients sitting in the waiting area have exactly what you studied back in the library because that is all you can remember. In the likely case that they don’t, you’re screwed!

11:30 PM
Back at home now. Fresh pair of pajamas on after a warm, much needed shower. Stomach is satisfied, the room is quiet. This is THE IDEAL time to study. You open up your books and identify the chapters that need to be covered before the night is over.

11:45 PM
You’re desperately trying to fight the inevitable…. Flipping through pages without even reading them. And then that little voice in your head gives in. “Who are you trying to kid buddy?” ………

11:50 PM
……

11:52 PM
….........………..

11:57 PM
zZzzZzzzZZZzz!

Does some of the above sound familiar to you? It should if you’re a senior med student. Ahhh, alas. SENIOR YEAR! Congratulations, you’ve finally made it. Only one more year to go. WOOO HOOOO…… NOT!!! This is more like the biggest reality check of your life. It feels like somebody just hit you in the face with a time machine brick and the clotting factors are just not kicking in. Dang that Christmas factor!! Time is going neither too slow, too fast, or just right. It’s just wrong! All wrong! Haha.

What I’m trying to say here my fellow colleagues and friends, is that it’s time to saddle up. In approximately one year’s time, you will be a certified doctor. Thaaaaat’s right. Patients will be your customers, and your brain is what’s in demand. Remember all that nonsense you said in your interview to get into med school?? “I want to become a doctor so I can help the sick”. HAHAHAHA. I gotta say, that sounds like something I said decades ago.

All jokes aside though, I think it’s prudent to remember why exactly we decided to slave ourselves for such a profession. As corny as this may sound, our patients need our patience. And this starts way before they step into our clinics. In fact, it started the day we entered medical school, if not earlier. It’s a tough life, but if you ask me (and yourselves for that matter), the rewards are indescribable. Knowing that you eased somebody illness is a high in itself. Not to mention if you’re honored enough to save a patient’s life. Talk about cloud 9 right?

This post was just a simple reminder to everyone (and mainly myself) that the hard work pays off. Our patients need it, and more importantly, I think we ourselves need it. Self satisfaction always trumps any paycheck. Sometimes we just need to sit back, gulp down a mug of coffee, maybe even two, and give ourselves a very much needed and well deserved pat on the back. Everything’s going to be just fine.

Good luck to all medical students around the globe with a special shout out to the senior med students of ZMU, class of 2010!

Pathology- MCQ's in Kids

2010-01-17T19:55:00.006+05:00

1) After four days, a neonate has not passed meconium, and begins vomiting. Physical examination reveals abdominal distension. Which one of the following is the correct diagnosis?

A. Hirchsprung's disease
B. Meckel's diverticulum
C. Omphalocele
D. Renal agenesis
E. Tracheoesophageal fistula

The correct answer is A. Hirchsprung's disease is caused by an absence of ganglion cells in both the submucosal and inter-myenteric plexus of a segment of bowel. The aganglionic bowel segment is narrowed because the lack of peristalsis keeps stool from moving into that segment. The distal rectum is always involved with the the lesion extending proximally. The bowel proximal to the lesion is usually dilated. Treatment is by surgical removal of the segment.

Meckel's diverticulum (choice B) is a small, usually asymptomatic pouch located near the ileocecal vale.

An omphalocele (choice C) would present with and obvious sac filled with intestines at the site of a defect in the ventral abdominal wall.

Reneal Agenesis (choice D) would present with failure to pass urine.

Tracheoesophageal fistula (choice E) would present with aspiration during feeding.

2) A 3 year old child develops headaches and is brought to the family doctor. Fundoscopic examination reveals papiledema; one retina also shows a very vascular tumor. CT of the head demonstrates a cystic tumor in the cerebellum. This child has a high likelihood of later developing which of the following?

A. Berry aneurysm of the basilar system
B. Bilateral renal cell carcinoma
C. Cancer of peripheral nerve
D. Choreiform movement related to decreased GABA and acetylcholine
E. Serum Cholesterol of greater than 700 mg/dL

The correct answer is B. The disease con Hippel-Landau disease, which is associated with a deletion involving the VHL gene on chromosome 3 (3p). Affected individuals develop vascular tumors (hemangioblastomas) of the retina, cerebellum, and/or medulla. Roughly half of the affected individuals later develop multiple, bilateral renal cell carcinomas.

Berry aneurysms (choice A) are unrelated to hemangioblastomas, but are instead associated with adult polycystic disease.

Peripheral nerve cancers (choice C) are a feature of von Recklinghausen's disease.

Choreiform movement, related to decreased GABA and acetylchline (choice D), are a feature of Huntigton's disease.

Extremely high serum cholesterol (choice E) suggests the homozygous form of familial hypercholesterolemia.

3) A 2 year old boy is brought to the pediatrician for a fever. The physical exam confirms a fever, but no source is identified. Generalized lymphadenopathy is also noted. She is admitted to a local hospital for observation. One day later she begins to have swelling of her knees and elbows bilaterally with rubor but no rash. Her liver and spleen are found to be slightly enlarged. Which of the following is the most likely diagnosis.

A. Felty's syndrome
B. Henoch-Schonlein purpura
C. Kawasaki's disease
D. Septic arthritis
E. Still's disease

The correct answer is E. Still's disease, or juvenile rheumatoid arthritis, affects children younger than 16 years old, usually 1-3 years of age. There is a female predominance. Both small and large joints are affected. The systemic onset of disease usually includes high fever, splenomegaly, general lymphadenopathy, and neutrophilic leukocytosis. A rash may or may not be present. Rheumatoid factor is usually negative, but if positive, it is associated with a poorer prognosis.

Felty's syndrome (choice A) is a polyarticular rheumatoid arthritis associated with splenomegaly, leg ulcers, and leukopenia (rather than leukocytosis). It affects adults with known rheumatoid arthritis or SLE.

Henoch-Schonlein purpura (Choice B) is a disease preceded by a respiratory infection and is characterized by vasculitis that affects the joints, skin, GI tract and kidney.

Kawasaki's disease (choice C), or mucocutaneous lymph node syndrome, is a vasculitis that occurs in children and causes fever, conjunctivitis, erosion of the oral mucosa, lymphadenopathy, and a rash. The most serious sequelae are due to coronary and aortic vasculitis.

Septic arthritis (choice D) is usually caused by hematogenous seeding of a joint during bacteremia. It usually affects children. Clinically, the joint is tender and swollen. Lymphadenopathy and fever are common. The joint affected is usually single rather than bilateral and there is no hepatosplenomegaly.

4) A 3 year old boy with an enlarging, left-sided, abdominal mass undergoes diagnostic biopsy. The tumor reveals a variety of cellular patterns: dense immature islands of epithelial cells, ribbons of spindled fibroblast-like stroma cells, and poorly formed tubular structures. This triphasic hisology is most suggestive of which of the following childhood neoplasms?

A. Embryonal Rhabdomyosarcoma
B. Ewing's Sarcoma
C. Hodgkin's disease
D. Neuroblastoma
E. Wilms' tumor

The correct answer is E. Wilms' tumor, a neoplasm of embryonic renal blastoma, contains both a neoplastic epithelial and stromal components.

Rhabdomyosarcoma (choice A) is a malignancy of skeletal muscle origin, and the cells are recognized by their cytoplasmic and eosinophilic muscle proteins (thin and thick filaments).

Ewing's sarcoma (choice B) appears as a monotonous mass of primitive, small, round cells with a thin rim of clear cytoplasm.

Hodgkin's disease (choice C) is a lymphoid malignancy that presents with lymphadenopathy, typically in the cervical or mediastinal nodes. The cellular components contains varying amounts of inflammatory cells and Reed-Sternberg cells.

Neuroblastoma (choice D) frequently presents as an abdominal mass in children; however, it does not have an epithelial component. The cell population of neuroblastoma ranges from primitive, small, blue, round cells to well-differentiated neuritic cells resembling ganglion cells.

5) A 6 month old child is evaluated by a pediatrician for growth failure and particularly foul-smelling stools. Studies demonstrate and elevated sweat chloride concentration. The child is placed on oral enzyme supplementation and begins to grow. Damage to which of the following organs would be most likely to lead to this child's death during early adulthood?

A. Heart
B. Large intestine
C. Liver
D. Lungs
E. Small intestine

The correct answer is D. Formerly, patients with cystic fibrosis usually dies of malnutrition. The use of oral pancreatic enzyme supplements have markedly changed the course of this disease, and death in the first few years of life is now uncommon. Unfortunately, damage to the the lungs in the form of multiple episodes of pneumonia leading to bronchiectasis and pulmonary fibrosis remains the major cause of mortality in the second and third decades.

The heart (choice A) is not damaged directly by cystic fibrosis, but pulmonary hypertension secondary to pulmonary fibrosis can cause right-sided heart failure.

Life-threatening disease of the large (choice B) or small (choice E) intestines does not usually occur in cystic fibrosis.

The liver (choice D) is also affected by cystic fibrosis, with intrahepatic bile plugs and extrahepatic biliary structures, leading in some cases to portal hypertension and biliary cirrhosis.

Swine Flu

2009-10-15T20:32:00.010+06:00

Swine flu outbreaks have always been common - except known to occur only among pigs. However, this recent strain that we has caused so much damaged amongs humans is a variant or a subtype of influenze A (h1N1).

First detected among the people of United States of American in April 2009, this virus is rapidly spreading via human-to-human contact in fear of which the WHO has already issued a warning that a pandemic of H1N1 may be fast approaching. Infact, currently the WHO has maintained a level 5 alert for a Swine Flu Pandemic!

Clinical Features?

Patients clinically present which quite the same features as common flu/cold or upper respiratory tract illneses.

Rhinorrhea or nasal congestion;

Fever;

Cough;

Sore throat;

Bodyaches/malaise;

Chills and
Diarrhea and vomitting may even be present!

How dangerous is H1N1 Swine flu?

According to analysis, most people who contracted Swine Flu have recovered without hospitalizations, complications and even medical treatment. However, some have met their deaths due to this condition.

People who are classified in the high risk group are;

Young children

Immunocompromised individuals

Pregnant women

Diabetics

Heart or kidney disease patients

Asthma patients

Neurocognitive or neuromuscular disorder patients

People who live near the areas where Swine Flu cases have been confirmed to exist

*Interestingly, people older than 65 years are least likely to get infected by Swine Flu because more fraction of them have acquired the antibody against H1N1 virus!

*Deaths have usually occured due to complicated respiratory illness causes like pneumonia, respiratory failure and acute respiratory distress syndrome.

Period of Infectivity?

A person may infect others 1 day before getting sick till about 5-7 days after the symptoms appear. This, ofcourse, can be varied from individual to individual.

*H1N1 virus can survive on environmental surfaces for 2 to 8 hours long and therefore may infect individuals during this time period.

*It is killed by heat ( 75 -100°C) and several chemical germicides (Hydrogen Peroxide, Cholrine, Iodine based products and alcohol)

Which investigations to undertake?

Respiratory Secretion Analysis - usually the specimen is obtained from nasopahryngeal aspirate

A real-time RT-PCR for Influenza A - which will test positive strongly for Influenza A and negative for H1 and H3.

Immunoflourescence (DFA or IFA) tests

Isloation of H1N1 by viral culture - usually not preffered as it takes too much time.

Treatment options?

Suspected cases

Treat with zanamivir alone or with a combination of oseltamivir and either amantadine or rimantadine as soon as possible after the onset of symptoms and for a duration of 5 days.

Confirmed cases

Zanamivir or oseltamivir should be administered for 5 days.

Pregnant women

Antiviral medications are in Pregnancy Category C, so they should be used during pregnancy only if the potential benefit outweighs the potential risk to the embryo or fetus.

Children younger than 1 year

Infants with swine influenza A (H1N1) are likely to have better prognosis if put on oseltamivir.

STAR SIGNS - if appear; you need to seek URGENT medical help!

In children:

Fast breathing rater or labored breathing

Cyanosis

Inability to drink

Drowsiness

Re-appearance of flu-like symptoms with worsening condition

Fever accompanied by a rash

In adults:

Dyspnea

Pain or pressure in chest/abdomen

A sudden attack of dizziness

Confusion

Severe persistent vomiting

SIMPLE WAYS THAT CAN SAVE YOU FROM SWINE FLU:

First step remains the newly generated Swine Flu vaccine that can efficiently prevent the flu. Both live, attenuated and inactivated influenza A (H1N1) 2009 monovalent vaccine formulations are available.

The dozes are:

Children aged 6 - 9 years: 2 shots separated by 4 weeks

10 years or Older: A single shot

Cover your nose and mouth with a tissue when you cough or sneeze. Throw the tissue in the trash after you use it.

Wash your hands often with soap and water. Or an alcohol based hand sanitizer.

Avoid touching your eyes, nose or mouth.

Limit close contact with sick people.

Try to avoid going out when you are sick!

Resources: Medscape/CDC/eMedicine; the article shall be updated as new information pours about Swine Flu - as most of the studies are underway regarding this disease.

*Goodluck avoiding Swine Flu!

Deviated Nasal Septum

2009-10-07T23:44:00.002+06:00

Vaccination Schedule according to WHO and EPI

2009-07-31T23:47:00.002+06:00

*just remember the only difference between both of these schedules is that in EPI, you cannot administer DPT after 2 years in a child.
In WHO, DPT can be given to children up to the age of 6 years.

*if measles is an epidemic, a child can be given the measles vaccination at 6-7 months. It is not recommended to give before this age mainly because the child has preformed antibodies from the mother. Do remember to make a note on giving the child measles vaccination, and make sure to still follow up with vaccinating with measles at 12 and 18 months.

*if a child is malnourished, measles vaccination is allowed to be administered at around 5 and a half to six months. But again, do make a note on giving the child this vaccination, and make sure to follow up with administering measles at 12 and 18 months.

The schedule thus is as follows:

Birth- OPV0, BCG
6 weeks- OPV1, Pentavalent 1 (DPT1, HepB1,Hib1)
10 weeks- OPV2, Pentavalent 2(DPT2, HepB2,Hib2)
14 weeks- OPV3, Pentavalent 3 (DPT3, HepB3,Hib3)
12 months-measles
18 months-measles.

*pentavalent vaccine consists of DPT, Hep B and Hib.

Examples:

1- A mother comes with 18 month daughter with no vaccinations, except for NID.
-start with BCG, give OPV1 and Pentavalent 1, and measles 1. Follow child as according to schedule, after every 4 weeks. only give measles 2 after 6 months of having recieved measles 1.

*Remember to still give OPV as EPI and WHO do not clash with the NID.

2-3 years according to EPI schedule?
-first contact, BCG, OPV1, Measles 1. Do not give Pentavalent as according to EPI DPT cannot be given to the child who is above the age of 2 years. Parents will have to get Hep B, Hib and DT seperately.

NOTE- Diarrhea does not contraindicate vaccinations. If OPV is administered at 4 weeks and a child has diarrhea, ask the mother to bring the child back 2 weeks later for another does of OPV. The child should be followed up for next vaccinations after 2 more weeks as scheduled for following vaccinations. Also, always make a note of vaccinations adminstered.

DIABETIC KETOACIDOSIS (DKA)

2009-07-24T11:35:00.003+06:00

DEFINITION:

Diabetic keto-acidosis (DKA) is a state of inadequate insulin levels resulting in high blood sugar and accumulation of organic acids and ketones in the blood. It is also common in DKA to have severe dehydration and significant alterations of the body’s blood chemistry.

WHO’S THE PATIENT: usually a type I diabetic
Could be a yet undiagnosed diabetic
or a known diabetic non-compliant on drugs
or a known diabetic who skipped his insulin because of history of diarrhea and vomiting

SIGNS AND SYMPTOMS:

Systems affected : CNS, respiratory, gastrointestinal and excretory
CNS:
1. lethargy
2. anorexia
3. coma
RESPIRATORY:
1. Ketotic breath
2. Air Hunger / Kussmall breathing
GASTROINTESTINAL:
1. Vomiting (in 2/3rds of patients)
2. abdominal pain, severe enough to be called pseudoappendicitis of DKA
3. polydipsia
EXCRETORY:
1. dehydration
2. polyuria

DIAGNOSTIC INVESTIGATIONS:

Hyperglycemia, ketonemia and hypercapnea are the significant findings. So we do the following laboratory investigations:
blood and urinary glucose, urinary ketones
urea, creatinine and electrolytes
HCO3
ABG
osmolality
serum lipid profile
CBC
serum amylase
culture and sensitivity (if signs of infection)

DIFFERENTIAL DIAGNOSIS:
Insulin reaction – exclude by administering 50ml of 50% glucose, condition will improve if it is an exogenous insulin reaction, if not then too no harm is done by the administered glucose.
salicylate poisoning – there will be history of aspirin (or some other salicylate) overdose.
lactic acidosis
hyperglycemia
hyper osmolar state
non – ketotic coma
advanced renal failure

TREATMENT:
1. Infuse normal saline through the same vein that’s used for taking blood sample, as this is an emergency. Replace 4-8 L in first 24 hours of onset. When glucose levels are 200mg, start orange juice and/or 5% saline to the normal saline.
2. Administer insulin, both subcutaneously and IV, giving 200 units in first 3 hours. You may give up to 10,000 units in first 24 hours.
if the patient has low potassium levels, demonstrated by a flattened or inverted T wave and prolonged QT interval, start potassium infusion in the 2nd or 3rd hour. Do not exceed 20 mEq/hr, giving up to 80 mEq in the first 24 hours.
3. Gastric lavage may be done, to prevent any aspiration.

If the DKA is severe, then monitoring of glucose, carbondioxide and acetone levels should be done every 2 hours, otherwise every 4 hours.

THE STABLE PATIENT:
The patient is said to be stabilized when his blood glucose is <200mg/100ml,>

Never Be Sick Again!

2009-07-02T20:06:00.006+06:00

Supracondylar Fractures of the Humerus in Children

2009-06-25T21:47:00.007+06:00

Anatomy:

The distal humerus resembles a triangle, with the medial and lateral columns making up the sides and the trochlea forming the base (270° arc). The lower end of the humerus is expanded from side to side, and has articular and non-articular parts. The articular part includes the Capitulum which articulates with the head of the radius and the Trochlea which articulates with the trochlear notch of the ulna. The non-articular part includes: the medial epicondyle (related to the ulnar nerve), the lateral epicondyle, the medial and lateral supracondylar ridges, the coronoid fossa, the radial fossa, and the olecranon fossa.

Supracondylar fractures of the humerus are common in young age. They are produced by a fall on the outstretched hand. The distal fragment is mostly displaced backwards, so that the elbow is unduly prominent, as in dislocation of the elbow joint. However, in a fracture, the three bony points of the elbow form the usual equilateral triangle.

Ossification:
The humerus ossifies from one primary center and 7 secondary centers. The primary center appears in the middle of the diaphysis during the 8th week of development.
The upper end ossifies from 3 secondary centers: one for the head, one for the greater tubercle, and one for the lesser tubercle. These 3 centers fuse together during the sixth year to form one epiphysis, which fuses with the shaft during the 20th year. The upper end is the growing end of the humerus.

The lower end ossifies from 4 centers which form 2 epiphysii. The centers include: one for the capitulum and the lateral flange of the trochlea (first year), one for the medial flange of the trochlea (9th year), and one for the lateral epicondyle (12th year). All three fuse during the 14th year to form one epiphysis, which fuses with the shaft at about 16 years. The center for the medial epicondyle appears during 4-6 years, forms a separate epiphysis, and fuses with the shaft during the 20th year.

Supracondylar Humeral Fractures:

Much of the difficulty encountered in treating distal humerus fractures lies in the complex anatomy of the elbow joint. The highly constrained nature of the elbow joint causes it to absorb energy following direct trauma. Consequently, articular comminution may occur.
The following observations were made in a study by Wilkins studying 4,520 fractures:
1) 97.7% of the fractures were of the extension type, and only 2.2% were of the flexion type; 2) most occurred in males and especially in between the ages of 5 and 8 years; 3) Volkmann’s ischemic contracture occurred in 0.5% of the fractures; and 4) the radial, median, and ulnar nerves were involved in that order of frequency.

Dameron has listed, depending on the type of fracture, four basic types of treatment: 1) side arm skin traction; 2) overhead skeletal traction; 3) closed reduction and casting, with or without percutaneous pinning; and 4) open reduction and internal fixation.

Classification:
Most distal humerus fractures can be classified into 2 etiologic groups: those resulting from a high-energy mechanism, such as a motor vehicle accident, and those resulting from a low-energy injury, such as a fall while walking.

Gartland has proposed a further classification for supracondylar fractures: Type I, undisplaced; Type II, displaced with intact posterior cortex; and Type III, displaced with no cortical contact; his classification also notes whether the fracture is displaced posteromedially or posterolaterally.

The type I undisplaced fracture can be satisfactorily treated closed with external fixation, such as a plaster cast. The type II fracture is displaced and is difficult to reduce and to hold reduced by external methods. The type III fracture is displaced posteromedially or posterolaterally with no cortical contact and the periosteum may be stripped; reduction is difficult, and maintaining reduction is almost impossible without some form of internal fixation. The fracture should be reduced in extension and reduction should be maintained through the use of the triceps bridge by holding the elbow in flexion if the pulse and vasculature tolerate it.

Angular Deformities associated with Supracondylar Humeral Fractures:

Previously cubitus varus or cubitus valgus were thought to occur because of growth arrest of the distal humeral epiphysis, rather than because of malreduction of the fracture.

Cubitus varus is the most common angular deformity that results from supracondylar fractures in children. Cubitus valgus, although causing tardy ulnar nerve palsy, is rarely seen and occurs more often from nonunion of lateral condylar fractures.

Cubitus varus and cubitus valgus should be prevented by obtaining proper anatomic reduction. Of the two, cubitus varus produces a distasteful cosmetic deformity, yet only rarely any limitation of motion. A big problem noted in the prevention of these abnormalities is obtaining satisfactory roentgenograms to determine whether any cubitus varus or valgus is present.

The three most common reasons for residual cubitus varus or valgus deformity are:
1) the inability to interpret poor roentgenograms and therefore, acceptance of a less than adequate reduction; 2) the inability to interpret good roentgenograms because of a lack of knowledge of the pathophysiology of the fracture; 3) loss of reduction.
Whether external mobilization or pin fixation is used, the forearm should be placed in the pronated position to decrease the lateral tilt and resultant cubitus varus.

Imaging Studies:

The bone quality, fracture pattern, level of comminution, articular involvement, displacement, and associated injuries, must be understood completely before treatment is attempted. Multiplane radiographs, including anteroposterior (AP) and lateral views, are appropriate.

AP radiographs should be obtained with the elbow flexed approximately 40° and with the radiographic beam directed perpendicular to the distal humeral surface. This allows disengagement of the olecranon from its fossa and permits a better view of the distal humerus.

In the pediatric population, the Baumann angle (the angle between the lateral condylar physeal line and the axis of the humerus) is often measured using AP radiographs. It must be compared to the contralateral side.

A computed tomography (CT) scan can be obtained of the distal humerus to further analyze the fracture pattern. Duplex Doppler ultrasonography or angiography can be performed to check vascular status.

Closed Reduction and Percutaneous Pinning:

Closed reduction is difficult not only to achieve, but also to maintain because of the thinness of bone of the distal humerus between the coronoid and olecranon, where most supracondylar fractures occur.

Fowles and Kassab noted that ulnar nerve lesions are common in displaced flexion fractures. The reduction is more difficult, the results are worse than in extension fractures, and these anteriorly displaced fractures should be considered for accurate reduction and percutaneous pinning.

Percutaneous fixation after closed reduction has the advantage of providing excellent stability of the supracondylar fracture in any position of the elbow. However, the ultimate result will be only as good as the initial reduction, and does not depend on the placement of the pins. If the fracture is not satisfactorily reduced and is held in an unsatisfactory position with pins, the outcome will be unsatisfactory, just as if no pin fixation were used.

A 5-year-old girl fell onto her outstretched hand and sustained a Gartland Type II supracondylar humerus fracture with medial impaction. (A) Lateral preoperative radiograph. (B) Anterior/posterior (A/P) preoperative radiograph. (C) Lateral radiograph after closed reduction and percutaneous pin fixation (cross-wire technique). (D) A/P postoperative radiograph. (E) Lateral radiograph taken four weeks postoperatively. (F) A/P follow-up (4 wks) radiograph. There is good evidence of healing.

Technique:
Place the patient prone or supine on a fracture table. Prepare and drape the elbow. Outline the posterior triangle of the elbow joint (the medial and lateral epicondyles and the olecranon). Reduce the fracture by applying longitudinal traction, extending the fracture, and manipulating with the thumbs to correct lateral tilt, medial impactation, or posterior displacement. Flex the elbow to neutral. Crisscross two smooth Steinmann pins through the condyles and metaphysic, one to exit above the medial epicondyle and one to exit above the lateral epicondyle. Be careful to avoid the ulnar nerve. Following engagement of the shaft, use an image intensifier to make sure the pin engages the opposite cortex proximally. Cut the pins off beneath the skin and bend their ends so they will not migrate proximally but can be easily retrieved in the office. Check and note radial pulse.

Aftertreatment:
A long arm posterior plaster splint is worn for 3 weeks. Ulnar, radial, and median nerve function should be checked after anesthesia. The pins are removed at 3 weeks and another posterior splint is applied. At 4 weeks, intermittent active range of motion exercises are started at home after being taught by a physical therapist to the child and parent. Passive motion or forceful manipulative motion must be avoided in children because they will decrease the range of motion and may frighten the child.

Open Reduction and Internal Fixation:

Open reduction and internal fixation of supracondylar fractures are indicated when closed reduction is unsatisfactory. In a type III displaced fracture with no cortical contact and completely detached periosteum, and with the fracture fragment penetrating the skin (compound fracture), a satisfactory closed reduction may not be possible, if, after one or two attempts at closed reduction with the child under general anesthesia, the fragments cannot be reduced and held by percutaneous pinning, open reduction and internal fixation are indicated. Also if the elbow is so severely swollen that a closed reduction cannot be maintained, then olecranon traction may be used for several days, followed by closed or open reduction as necessary. Other indications for O.R.I.F. include open (compound) fractures that require irrigation and debridement and those fractures complicated by vascular injury, mysositis ossificans excessive callus formation with residual stiffness, and decreased range of motion.

If open reduction and internal fixation are to be carried out, they should be performed after the swelling has decreased, but no later than 5 days after that time because the possibility of mysositis ossificans increases after that time.

Gruber and Hudson treated 31 difficult fractures with open reduction and internal fixation and observed satisfactory results even in the most severe ones.

Technique:
Prepare and drape the arm in the usual fashion with the patient supine. Make a curved incision over the lateral humeral epicondyle. Dissect the soft tissue, including the anconeus and common extensor origins, and retract these anteriorly and posteriorly respectively. Make sure the radial nerve is retracted posteriorly to avoid injury. Observe the supracondylar fragment, and note its alignment with the proximal fragment. Use a small curet to remove any hematoma at the fracture site. Note any interdigitations on the ends of the bone and by matching them, reduce the fracture. Use two crossed Steinmann pins in a manner similar to that described for percutaneous pinning. Cut the pins percutaneously for easy removal later. Close the incision in layers.

Aftertreatment:
A posterior plaster splint is applied and the radial pulse and neurological function are checked following anesthesia. The pins are removed at 3 to 4 weeks and an active, not passive, range of motion program is started.

Complications:

Supracondylar fracture of humerus being the most common fracture in children needs proper treatment to prevent complications like compartment syndrome, neurovascular compromise (Volkmann’s ischemic contracture), elbow stiffness (mysositis ossificans) and angulations.

Injuries to nerves or blood vessels are much more serious than the fracture itself. The early recognition of such complications is imperative. Early and adequate treatment of acute vascular complications is necessary, even though it means surgical exploration of the antecubital fossa and resection of the injured segment of the brachial artery. Adequate and early treatment of acute vascular injuries usually ensures a good prognosis, but delay may lead to serious and permanent disability.

Gartland type I supracondylar fracture can be early treated with casting alone but displaced (Gartland type II, III) can be treated with casting, ORIF or percutaneous Pinning (PCP). Close reduction and casting is an old treatment modality that is still practiced in developing countries due to limited facilities. Close reduction and casting has its own advantages and disadvantages. Its advantages are no need of metal insertion, least costly, safe, time effective, bearing less morbidity. Disadvantages are loss of reduction, compartment syndrome and cubitus varus.

References:

Campbell’s Operative Orthopedics, 4 volume set
Human Anatomy: Regional and Applied. B.D. Chaurasia
www.emedicine.com
www.wikipedia.com

The Diabetic Patient: A Clinical Approach

2009-06-07T19:15:00.000+06:00

Diabetes Mellitus is a metabolic disorder affecting millions of people across the globe. We as doctors and medical students should know these patients from A-Z. The following is a quick review of points to remember when approached by someone with diabetes in your clinic.

History: Take a normal history as with any other patient, but keep these points in mind...

Hypoglycemia- tremors, fatigue, palpitations, sesting, coma
Neuropathy- calf muscle pain, burning muscles, "losing shoes"
Nephropathy- decreased urine output, frothy urine, periorbital swelling, recurrent UTI
Cardiovascular- pain, dyspnea, loss of breath
Retinopathy- blurry vision, halos, spots
Autonomic- orthostatic hypotension, GIT disturbances, recurrent infections
Dermopathy- poor wound healing

Investigations: (for the known diabetic)

Fasting blood sugar- <110>125 is established diabetes
Lipid profile- ALT and SGPT every 6 months
Urine DR in special regards for microalbuminuria (<200>200 is irreversible).
Creatinine clearance
Serum creatinine and Urea
ECG
Fundoscopy

Examinations: Perform foot, abdominal, CVS, respiratory, 3rd 4th 6th 7th cranial nerves, and check of dehydration.

Particularly in Foot examination:
Inspection- look for discoloration, ulcers, callus', skin changes, loss of shin hair, cuts, and bruises. Pay special attention to the intertarsal spaces.
Palpation- pedal edema, vibration (this is usually the first sense to be compromised in 'diabetic foot'- diabetic neuropathy), proprioception, temperature, touch, reflexes, pulses.

Diet: The following diet pertains particularly to those patients from the Indian subcontinent. Please refer to a diabetic book for patients of other ancestry.

Contraindications- bakery sweets, white bread, white a'ata (use chokaar instead), rust, cold drinks (sodas), sharbaats, gosht, biryani, mattar plow, biscuits, jam, jelly, honey, red meat.

Foods that help- chaana with chai, boiled eggs, akhroat, dhalia, omega 6 fatty acids (fish and walnut).

Keep in mind- eating 1/2 cup rice is okay but only once a day, oil should be decreased in all foods, dhai with no sugar or malai, only 1 fruit is allowed per day.

Management:
Management of diabetes varies from patient to patient. Please refer to medicine books for details.

Diabetic Emergencies:

Diarrhea and vomiting can cause uremia leading to hiccups.
Acute renal failure
Diabetic ketoacidosis- Patient is usually young with Type I DM.
Hyperosmotic nonketotic diabetic coma causes high bloog glucose levels and dehydration

Plasma osmolarity can be calculated by the following equation: (normal is 275-290 mmol)
Plasma osmolarity = (sodium x 2) + (BUN / 2.8) + (blood glucose / 18)

Managed initially by I/V insulin and isotonic saline. Followed by dextrose with insulin to allow for intracellular free water absorption.
Check blood pressure for orthostatic hypotension.

Further investigations: CBC, blood culture, urine culture, head to toe examination for signs of infection.

Note: The following was just a quick review of what to expect when dealing with a patient with known diabetes mellitus. Please refer to a textbook for further details.

Pathology- Female reproductive MCQ's

2009-06-01T23:10:00.004+06:00

1) Which one of the following endometrial lesions is associated with the highest risk of developing endometrial carcinoma?

A. Chronic endometritis
B. Complex hyperplasia with atypia
C. Complex hyperplasia without atypia
D. Simple hyperplasia
E. Squamous metaplasia

The correct answer is B. In general, any condition characterized by excessive estrogenic stimulation is associated with some degree of endometrial hyperplasia and increased risk of endometrial cancer. Endometrial hyperplasia is a histologic precursor of endometrial adenocarcinoma.The most severe changes are present in complex hyperplasia with atypia. Disorganization and crowding of glands, high mitotic activity, and nuclear atypia characterize this change. 25% of women with this form of hyperplasia develop adenocarcinoma.

2) a 36 year old gravid female notes vaginal bleeding. Ultrasound reveals small grape-like cystic structures witout evidence of a developing embryo. A diagnosis of complete hydatidiform mole is made at the hospital. Further analysis is most likely to reveal that:

A. hCG levels are markedly increased
B. serum levels of alpha fetoprotein are elevated
C. the genotype of the mole is 46,XX and is completely paternal is origin
D. the genotype of the mole is triploid
E. two or more sperm fertilized the ovum

The most correct answer is C. A complete hydatidiform mole is characterized by elevated hCG and grape like cystic structures filling the uterus with no detectable embryo on ultrasound. The genotype of a complete hydatidiform mole is purely paternal, caused by fertilization of an egg that has lost its chromosomes. Hydatidiform mole is associated with increasing maternal age, and may be a precursor to choriocarcinoma.

hCG levels are increased relative to normal values for dates, rathar than decreased, in a molar pregnancy (choice A).

Alpha fetoprotein (choice B) is a marker for endodermal yolk sac tumors, embryonal tumors in men, and hepatocellular carcinoma. It is made by the fetus, hence not detectable in a complete hydatidiform mole.

Triploidy and even tetraploidy are characteristics of partial moles (choice D). Partial moles are thought to be due to fertilization of an egg with two different sperm, one with an X and one with a Y chromosome, typically leading to triploidy.

Two or more sperm may fertilize an ovum, leading to a triploid fetus and a partial mole (choice E).

3) A 37 year old woman complains to her gynecologist of discomfort during intercourse and placement of a tampon. Physical examination demonstrates flocculent swelling below the skin of the posterolateral part of one labium majora. Which of the following is the most likely diagnosis?

A. Bartholin's gland cyst
B. Condylomata acuminatum
C. Lichen sclerosis
D. Vestibular adenitis
E. Vulvar squamous hyperplasia

The correct answer is A. This is a Bartholin's gland cyst, which is a relatively common lesion occurring when Bartholin's duct becomes obstructed, typically a sequela to a previous infection. The cysts can enlarge to 3 to 5 cm in diameter.They are lined by either transitional or metaplastic squamous epithelium. Treatment is by excision or marsupialization (permanent opening).

Condylomata acuminatum (choice B) usually produces a papillary lesion (venreal wart).

Lichen sclerosis (choice C) usually produces gray, parchment-like thinned epidermis.

Vestibular adenitis (choice D) usually produces an exquisitely tender posterior introitus with focal ulcerations.

Vulvar squamous hyperplasia (choice E) usually produces a white plaque.

4) A 39 year old woman has cyclical premenstrual pain. Her breasts have a "lumpy bumpy" texture on palpation. A biopsy is performed. The histopathologic features include small cysts lined by epithelial cells with apocrine metaplasia, calcium deposits, areas of fibrosis, increased number of acini (adenosis), and foci of florid hyperplasia of ductal epithelium. Which of these changes increase the risk of breast cancer?

A. Adenosis
B. Apocrine metaplasia
C. Calcium deposits
D. Cysts
E. Epithelial hyperplasia

The correct answer is E. Fibrocystic changes usually come to clinical attention by causing pain (often cyclical, in premenstrual phase), palpable lumps, or mammographic densities and calcifications. A "lumpy-bumpy" texture is caused by cysts and fibrosis. Epithelial hyperplasia is defined as an increase in the number of epithelial cell layers in the ductal epithelium. Florid epithelial hyperplasia leads to an increased risk of developing carcinoma, especially is these is associated cellular atypia (atypical ductal hyperplasia).

Adenosis (choice A) refers to an increase in the number of acini and can be observed in fibrocystic changes as well as in other breast conditions, such as sclerosing adenosis.

Apocrine metaplasia (choice B) describes a benign change of breast epithelial cells that come to resemble the apocrine epithelium of sweat glands.

Calcium deposition (choice C) is a nonspecific finding that mar occur in a number of both benign and malignant breast change, including fibrocystic changes, ductal carcinoma in situ, and invasive carcinoma. Calcification is not clinically significant except for its diagnostic value.

Cysts (choice D) are frequent in fibrocystic changes and result from dilatation of ducts. A classic gross description is that of blue-dome cysts, which appear brown to blue because of their turbid fluid content.

5) An 83 year old female has a biopsy of an ulcerated nipple lesion that is interpreted as Paget's disease. A biopsy of the underlying breast tissue will most likely show which of the following?

A. Acute mastitis
B. Ductal carcinoma in situ
C. Intraductal papilloma
D. Invasive lobular carcinoma
E. Normal breast tissue

The correct answer is B. Paget's disease of the breast is a form of ductal carcinoma in which neoplastic cells involve the squamous epithelium of the skin by direct extension through the lactiferous ducts.

Acute mastitis (choice A) is a disease of nursing women in which bacteria (S. aureus) gain entry to the breast tissue via cracks in the traumatized nipple. It is characterized by acute inflammation and tissue necrosis.

Intraductal papilloma (choice C), a papillary mass arising within the ducts, usually presents as a single subareolar tumor that may produce a bloody or serous nipple discharge.

Invasive lobular carcinoma (choice D) is a tumor of the terminal ductules of the breast. It presents as a poorly circumscribed, rubbery breast mass. Lobular carcinoma does not produce Paget's disease.

Paget's disease of the breast always reflects underlying ductal cancer. This is in marked distinction from extramammary Paget's disease, which may arise without an identifiable malignancy (choice E).

GLAUCOMA

2009-04-13T07:06:00.003+05:00

Glaucoma: group of diseases in which increased IOP (intraocular pressure) in an eye produces optic disc cupping and visual field defects.

Normal IOP: 10-21 mm Hg
- Usually slightly high in the morning and slightly deceased at night.

PRODUCTION OF AQUEOUS HUMOR:
(a) Active Secretion: 80% ultrafiltration & 20% diffusion
(b) Drainage: 90% through the Trabecular pathway & 10% through the Uveo-scleral pathway
(c) Level o episcleral venous pressure

CLASSIFICATION:
A. Developmental aka. Congenital: Children present with BUPTHALMOS (increased corneal diameter)
- Primary
- Rubella
- Secondary to other ocular causes such as aniridia
B. Acquired
1. Open angle
- Primary – chronic open angle
- Secondary
2. Closed angle
- Primary – Acute and Chronic closed angle
- Secondary – Due to trauma, raised episcleral venous pressure, steroid induced, associatd with other ocular disease such as uveitis

TONOMETRY (measurement of tension or pressure, particularly IOP)
1. Goldmann tonometer
2. Schiotz tonometer
3. Perkin’s tonometer
4. Air Puff tonometer
5. Tono pen

EYE EXAM:
1. Check IOP
2. Look for optic disc cupping
3. Test field of vision

GONIOSCOPY (examination of anterior chamber of the eye to demonstrate ocular motility and rotation)
- Done to identify structures in the irideo-corneal angle.
- Use a triple-mirror GONIOLENS to visualize the angle and the periphery of the retina
- Opening of the angle is graded (Grades 0-4)
Grade 0: Closed angle
Grade 1:Narrow angle
Grade 2: Moderately narrow angle
Grade 3: Open angle
Grade 4: Widest angle

OPTIC NERVE HEAD CHANGES SEEN IN GLAUCOMA:
1. Retinal nerve fiber changes
2. Concentric expansion of optic disc cup
3. Localized expansion of optic disc cup (notching at inferior or superior pole)
4. Narrowing of neuro-retinal rim
5. Pallor
6. Splinter hemorrhages on disc margin
7. Deepening of optic cup
8. Nasalization of vessels
Note: Papillomacular area is spared and tunnel vision is preserved!!

PERIMETRY:
Visual field: an island of vision surrounded by a sea of darkness.
Normal visual field:
- Superiorly 50 degrees
- Inferiorly 70 degrees
- Nasally 60 degrees
- Temporally 90 degrees

VISUAL FIELD DEFECTS SEEN IN GLAUCOMA:
1. Arcuate Scotomas
2. Isolated paracentral scotoma
3. Nasal step
4. Temporal wedge
5. Ring scotoma

PRIMARY OPEN ANGLE GLAUCOMA:
1. Adult onseT
2. IOP > 21mm Hg at some point in the course of the disease
3. An open angle of normal appearance
4. Glaucomatous optic nerve damage
5. Visual field defect

RISK FACTORS for the development of glaucoma:
1. Age > 40 years
2. Race (higher incidence in Black people)
3. Family history
4. Diabetes
5. Hypertension
6. Myopia
7. Prolonged use corticosteriods (oral or topical)

SYMPTOMS: Usually symptomless & diagnosed on routine eye examination!!
- Patient with Acute closed angle Glaucoma may present with : photophobia, and painful eye, loss of vision, watering of the eye

SIGNS:
1. Increased IOP
2. Fluctuating IOP
3. Optic disc changes
4. Glaucomatous field change

TREATMENT:
1. Medical :
- Alpha-2 agonists eg. Apraclonidine
- Beta Blockers eg. Timolol, Carteolol
- Carbonic anhydrase inhibitors eg. Brinzolamide, Dorzolamide
- Prostaglandins eg. Latanoprost, Travaprost
- Sympathomimetic and Parasympahtomimetic agents eg. Adrenaline, Pilocarpine

2. Laser cyclophotocoagulation

3. Surgery (has a lot of complications and is therefore the last resort of treatment!)
- Argon Laser trabeculoplasty
- Trabeculectomy (a fistula is created between the angle of the anterior chamber and sub Tenon’s space to allow drainage of the fluid)
- Cryotherapy of ciliary body

Management of TRABECUECTOMY FAILURE:
1. Adjunctive Antimetabolites- such as 5-FU and Mitomycin
2. Artificial drainage shunts
3. Cyclodestructive procedure using Lasers OR Cryotherapy

LOW-TENSION GLAUCOMA:
- Also known as Normotensive Glaucoma
- The intraocular pressure is normal but optic disc cupping and field defects are present

OCULAR HYPERTENSION: IOP > 21 mm Hg but there’s no cupping and visual field defects

Cataract

2009-04-12T19:24:00.004+05:00

Any congenital or acquired opacity in the lens capsule or substance, irrespective of the effect on vision, is a cataract. Cataract is the commonest cause of treatable blindness in the world.

Lens: The lens is biconvex and transparent. It is held in place behind the iris by the suspensory ligament whose zonular fibers are composed of protein fibrillin which attach its equator to the ciliary body. Disease may affect structure, shape and position.

Normal lens: 4-5mm thick and approx. 10 mm in diameter.
Outer: cortex.
Inner: Nucleus

Classification:
I. According to Age
- Congenital
- Infantile
- Juvenile
- Pre-senile
- Senile

II. According to Morphology
- Capsular
- Sub-capsular
- Cortical
- Nuclear

III. According to Etiology
- Age related: example senile cataract
- Traumatic cataract
- Metabolic cataract: due to diabetes mellitus, hypoparathyroidism
- Toxic cataract: due to use of steroids, and other medications
- Complicated cataract: secondary to some other eye disease such as chronic anterior uveitis, acute angle closure glaucoma, pathological myopia

IV. According to Maturity
- Immature cataract
- Mature cataract
- Hypermature cataract: Proteins are liquefied and the permeability of the capsule is increased. This results in leakage of proteins and deposition of calcium.

Example: MORGAGNIAN CATARACT (Cortex liquefies and the nucleus sinks down)

Intumescent cataract: Lens is swollen due to water retention. Maybe immature, mature or hypermature.

Symptoms:
1. Blurred vision (most important symptom)
2. Glare
3. Monocular diplopia
4. Haloes around light
5. Improvement in near vision

Signs:
Depend on the state of maturity of the cataract
1. Decreased visual acuity
2. Change in the colour of the pupil
3. Iris shadow
4. Abnormal red reflex

Management:
(There is no medical treatment for cataract!)
1. Surgery (Goal of cataract surgery: to leave the patient emmetropic)
2. Glasses

Indications for Cataract Surgery:
1. Visual improvement
2. Medical indication eg. The patient develops glaucoma or diabetic retinopathy,r etinal detachment
3. Cosmetic indication

Pre-operative Assessment:
1. Complete ocular exam
2. Macular function test
3. Optic nerve function test
4. Biometry
5. Investigations:
- CP & ESR (complete blood picture and erythrocyte sedimentation rate)
- FBS (fasting blood sugar)
- UDR (urine detailed report)
- Hep B and C virology

Anaesthesia:
1. Facial Block
2. Retrobulbar block

Surgical Techniques:
1. ECCE (Extra Capsular Cataract Extraction)
2. ICCE (Intra Capsular Cataract Extraction)- not used anymore
3. Phacoemulsification – the newest method

Disadvantages of ICCE (Intra Capsular Cataract Extraction):
1. Large incision
2. Posterior capsule is removed and so the vitreous gel may come out
3. Posterior capsule is removed and therefore, there is no support for the IOL (intraocular lens)

Advantages of Phacoemulsiication:
1. Small tunnel incision
2. Quick recovery
3. Early visual rehabilitation
4. Useful for the removal of soft cataract (nucleus is soft)

Complications of Cataract Surgery:
1. Operative complications
- Rupture of posterior capsule
- Vitreous loss
2. Post-op complications
- Iris prolapse
- Corneal edema
- Uveitis
- Endopthalmitis
- Post-op Astigmatism
- Cystoid macular edema
- Retinal detachment
- Posterior capsule opacification

Congenital Cataract
- Opthalmological emergency!!!!
- Bilateral congenital cataract results in a significant effect on visual acuity and results in nystagmus and amblyopia.
Nystagmus: involuntary rapid movement (horizontal, vertical, rotatory or mixed i.e. of two types) of the eyeball.
Amblyopia: dimness of vision without detectable organic lesion of eye.

Age-Related Macular Degeneration

2009-04-09T14:07:00.000+05:00

It is the leading cause of irreversible blindness in developed countries.
Complex multifactoral progressive disease with genetic and environmental influences.

PATHOGENESIS:
Not well understood but it is believed that oxidative stress is the key component of retinal pigment epithelial (RPE) degeneration. Progressive diffuse thickening of the Bruch's membrane (retinal layer that provides nourishment and oxygen to the RPE and the outer layers of retina, including the rod and cone cells) causes hypoxia----> choroidal neovascularisation---->weak new vessels leak serous fluid/blood---->distort central vision and reduce clarity of central vision.
Alternatively death and atrophy of RPE also occurs.

DRUSEN BODIES: visualized clinically as yellow deposits situated within Bruch's membrane. Vary in size and shape/maybe discrete or confluent. Either collagen-based or granular lipid rich.

ESSENTIALS OF DIAGNOSIS:
Older age group (>55year)
Gradual progressive simultaneous or sudden sequential deterioration of central vision in both eyes affecting reading and recognising faces.
Distortion or abnormal size of images (demonstrated by Amsler chart)
No pain or redness.
Macular abnormalities seen by ophthalmoscope.

Suggested Associated Risk Factors:
famale sex
smoking history
family history
hypertension
hypercholestrolemia
history of exposure to UV light
hypermetropia
cataract surgery

Dry ARMD/ Atrophic Degeneration 85%:
Gradual progressive bilateral visual loss of moderate severity.
Atrophy and degeneration of outer retina and RPE.
Variable and may result in severe visual impairment over a span of 5-10 years.
In advanced stages it is possible to see underlying choroidal vessels.

Treatment: No specific treatment but patients benefit from visual rehabilitation (refraction and low vision assessment). Peripheral fields and hence navigational vision are always maintained.

Wet ARMD/ Exudative Degeneration 15%:
Aggressive form of the disease.
Rapid clinical course and 75% of the patients have marked reduction in vision over 3 years.
Disease characterized by choroidal neovascularisation----> fluid leakage and bleeding in the macular region.

Treatment: is aimed at closing off blood flow through the area of choroidal neovascularisation to allow resolution of exudative changes. It is based on which of the following categories (as seen in Fundus Fuorescien Angiography) the disease falls in:
Classic only- neovascularisation fully delineated
Predominantly classic with little occult- ≥50% classic with some occult
Minimally classic- ≤ 50% but >0% classic
Occult only- full extent of neovascularisation not visible

Laser Photocoagulation: occludes neovascular regions of retina
Done for classic-extrafovealand juxtafoveal conditions but also causes considerable to adjacent retina.

Photodynamic Therapy: light activated agent, verteporfin, is given IV. Laser is then used at a particular wavelength to activate the photosensitizer which causes local vessel occlusion without damage to nearby retina. Needs to be repeated every 12 weeks.
This too is used for the subfoveal type of the classic lesion.

Antiangiogenic Agents:
Inhibitors of vascular endothelial growth factor(eg synthetic steriods) which would reverse neovascularisation.
Have to be administered every 4-6 weeks with risks of intraocular infection, inflammation and retinal detachment.
These can be used for both classic and occult.

Submacular Surgery:
Microsurgical viterectomy + retinal incision and then removal of vessels.
Suitable for selected cases.

Macular Rotation:
Macular region of retina is physically moved to overlie another place where the RPE is healthy followed by strabismus surgery. The procedure is complicated and carried significant risk.

Pathology- GIT MCQ's

2009-04-09T01:45:00.001+05:00

1) A 60 year old man presents to his physician because of progressive dysphagia, first for solids, then for liquids. Endoscopy reveals a large fungating mass 2 cm above the gastroesophageal junction. Biopsy of the mass demonstrates glands, extending into the muscular layer, containing cells with large hyperchromatic nuclei. Which one of the following conditions is most likely associated with the development of this mass?

A. Barrett's esophagus
B. Esophageal rings
C. Esophageal webs
D. Scleroderma
E. Sliding hernia

The correct answer is A. Biopsy is consistant with esophageal adenocarcinoma which usually arises in aread of gastric or intestinal metaplasia (Barrett's esophagus) in the lower or middle one third of the esophagus. The prognosis for adenocarcinoma is poor, unless caught very early.

Esophageal rings (choice B) are rims of fibrovascular tissue found in the lower esophagus.

Esophgeal webs (choice C) are mucosal ledges in the upper esophagus.

Scleroderma (choice D) can cause fibrosis and impaired motility of the esophagus.

In sliding hiatal hernias (choice E), part of the stomach protrudes above the diaphragm.

2) A 30 year old man with a 15-year history of ulcerative colitis develops intermittent cholestatic jaundice. Ultrasonographic examination fails to reveal gallstones. Liver biopsy demonstrates a large bile duct obstruction. Which of the following would most likely be seen on endoscopic retrograde cholangiopancreatography (ERCP)?

A. Beading of transhepatic bile ducts
B. Markedly dialted common bile duct containing irregular radioluscent masses
C. Mass at the ampulla of Vater
D. Moderately dilated intrahepatic bile ducts and stricture in the bile duct at the lower end of the common bile duct

The correct answer is A. The most likely diagnoses is primary sclerosing cholangitis, a disorder with a probable autoimmune component that is associated with ulcerative colitis (66% correlation). The disease is characterized by inflammation and fibrosis of the intrahepatic and extrahepatic bile ducts, producing alternating strictures and dilatation of the structures. These changes are seen as "beading" on ERCP.

Gallstones in the biliary tree produce irregular radiolucent masses (choice B).

Choice C describes the findings associated with carcinoma of the ampulla of Vater.

Choice D describes the findings associated with carcinoma of the extrahepatic bile ducts.

Choice E describes the findings associated with carcinoma of the pancreas.

3) A patient has had years of intermittent diarrhea and abdominal pain, but has never consulted a physician. Eventually he begins to pass fecal material in his urine and he seeks medical attention. Which one of the following diseases is most likely to cause this complication?

A. Celiac disease
B. Crohn's diease
C. Diverticulitis
D. Ulcerative colitis
E. Whipple disease

The correct answer is B. Passing fecal material in urine strongly suggests the possibility of a fistula between the bowel and bladder. Of the diseases listed, only Crohn's disease commpnly produces fistulas. Fistulas are produced in Crohn's disease because the disease affects the entire thickness of the bowel wall, rathar than being restricted to the mucosa (e.g., ulceratice colitis).

Celiac disease (choice A) is a mucosal disorder of the small intestine caused by intolerance to certain components of gluten from wheat and other grains.

Diverticulitis (choice C) can cause bowel perforation with peritonitis but does not usually cause fistula formation.

Ulcerative colitis (choice D) is much less commonly associated with fistula formation than is Crohn's disease.

Whipple's disease (choice E) is a small intestinal disorder caused by infection with Tropheryma whippelii.

4) A 40 year old man complains of increasing difficulty in swallowing in the past 3 years. He reports a feeling of pressure in the chest occurring 2-3 seconds after swallowing a solid bolus. He also experiences regurgitation of undigested food eaten hours previously. A radiograph taken after swallowing barium shows a distended esophageal body with a smooth tapering at the lower esophageal sphincter. Manometry shows the absence of esophageal peristalsis and a lower esophageal sphincter that fails to relax. What is the most likely diagnosis?

A. Diffuse esophageal spasm
B. Incompetent lower esophageal sphincter
C. Oropharyngeal dysphagia
D. Scleroderma
E. Achalasia

The correct answer is E. Achalasia is an acquired esophageal motility disorder that slowly develops. The motility is abnormal due to the loss of inhibitory enteric neurons of the esophageal body and lower esophageal sphincter. Both vasoactive intestinal peptide and nitric oxide function as inhibitory neurotransmitters here, and the presence of both is decreased in achalasia. Radiographs typically show a dilated esohpagus that tapers at the lower esophageal sphincter, producing the so called "bird's beak". Because of the poor motility, ingested food is regurgitated and can lead to aspiration symptoms. Manometric demonstration of absent peristalsis in the esophageal body and poor relaxation of the lower esophageal sphincter with a swallow confirm the diagnosis.

The primary complaint with diffuse esophageal spasm (choice A) is mid-sternal pain that can be misdiagnosed as cardiac pain. The pain is caused by prolonged contraction of the entire esophageal body. Symptoms can be brought on by eating certain hot or cold meals. A manometric study may show poor peristalsis in the smooth muscle portion of the esophageal body, but lower esophageal sphincter function is unaffected.

The primary complaint with incompetant lower esophageal sphincter (choice B) is heart burn and regurgitation due to gastroesophageal reflux. Endoscopic examination of the esophagus may reveal inflammation, erosions, and even ulcers. A manometric study would show lower than normal resting tone in the lower esophageal sphincter.

The fact that the patient's symptoms do not occur until 2-3 seconds after a swallow suggests that oropharyngeal dysphagia (choice C) is not the diagnosis. The presence of cogh, Hoarseness, or nasal regurgitation commonly occurs with this disorder. Oropharyngeal dysphagia is often due to neurological or muscle disorders like stroke, amyotrophic lateral sclerosis, muscular dystrophy, or myasthenia gravis.

Scleroderma (choice D) is a connective tissue disease in which esophageal smooth muscle is gradually replaced by dense collagenous material. Manometry woud show poor esophageal peristalsis and decreased lower esophageal sphincter tone. Significant acid reflux with resultant esophagitis is almost universal.

More questions to come soon...

Diabetic Retinopathy

2009-04-06T20:39:00.003+05:00

Diabetic Retinopathy is one of the commonest cause of blindness in the world. Diabetics are at 25% more risk to be blind than normal people. Also, almost half of the diabetics at some stage develop eye disease. Hence, diabetes is a major predisposing factors to ophthalmic pathology.

Ocular diseases that are associated with Diabetes include:

a- Diabetic Retinopathy
b- Cataract
c- Glaucoma
d- Infections

(Delayed healing is also a result of diabetes)

Pathogenesis:

The major factor in the pathogenesis of Retinopathy in diabetics is a microangiopathy of vessels supplying the retina )or a part of it(.

The main vascular damage can be divided into two parts: a) Leakage; b) occlusion

a) Endothelial cells rely exclusively on glucose for nutrition and insulin helps in the transport of glucose into them. Thus, when there is absence of insulin or a resistance to it, the cells start becoming undernourished. And overtime they suffer injury (and most likely cell death). The dead cells result in a leaky and weakened vessel wall. The leaky vessel wall leads to edema of the retina, followed by hemorrhage and finally WBC infiltration - thus resulting in damage to the retina.

b) As the vessel continues to weaken, microaneurysms form in the vasculature which over time can get occluded and thus lead to infarction of the retina supplied distally to the occlusion.
As the retina is denourished due to thrombosis of the vessel supplying it, there is release of Vascular Angiogenesis Factor (VAF). Under the influence of VAF, new blood vessels are formed to keep the retina nourished but that is to no avail as the new vessels leaky and weak and thus more hemorrhage and edema occurs, resulting in further loss of vision.

Risk Factors:

a) Duration of diabetes
b) Control of Diabetes
c) Pregnancy and other diabetogenic conditions
d) Anemia
e) Hypertension - DM and HTN go hand in hand
f) Smoking
g) Obesity and Hyperlipidemia

Symptoms:

This form of retinopathy is asymptomatic initially. Although some people might complain of dark areas in their vision.

Signs:

On Ophthalmic examination, red (hemorrhagic) and white (exudative) dots are seen. Exudates are of two types: hard and soft. Hard exudates contain protein, have marked edges and are small and discrete. the soft exudates on the other hand are of a lighter colour. They appear softer and have less marked edges with fuzzy borders.

Classification:

Diabetic Retinopathy are classified in two types depending on vascular proliferation. They are as follows:

a) Non-proliferative: they don't grow from the initial lesion and there is no neovascularization, or only minimal.

b) Proliferative: there is dangerous level of neovascularization and they appear as fronds. These vessels might bleed into the Vitreous and give rise to opaque membranous plaques which can then result in retinal detachment.
If all the above is present along with glaucoma, the condition is called Advanced Diabetic Eye DIsease (ADED).

Diagnosis:

It is based on positive history of Diabetes and Ophthalmoscopic examination.

Complications:

a) Vitreous hemorrhage
b) Retinal detachment
c) Formation of opaque membranes
d) Burnt-out stage

Treatment:

Specific: is to get rid of the new vessels being formed and removing the occlusion
Non-specific: control Diabetes and Hypertension; avoid ischemia

Screening:

Screening is an important tool in preventing the development of Retinopathy in cases with high index of suspicion. Diabetics should be examined at least once a year and the frequency should increase with every decade.

Common Nose Emergencies - Their Management.

2009-04-05T01:07:00.011+05:00

Foreign Body in the Nose? Outline your management.

History/examination

Plain X ray of the nose in lateral and anteroposterior view (when necessary)

Removal of the foreign body (depending on the type):

*Flattened FB (eg piece of paper) -----> Removal by pair of Crocodile forceps

*Ireggular rounded FB ------>Removal by a rounded Hook or Probe (do NOT attempt by Crocodile forceps as it may cause the fb to be lodged deeper in the nose).

Treating Epistaxis?

Pinching ---->if unresponsive-----> Anterioir Nasal Packing ---->if unresponsive--- >Posterior Nasal Packing ----->if unresponsive-----> Cautery by Silver Nitrate.

*the patients presenting with severe epistaxis must be immediately made hemodynamically stable by:

maintaining ABGs, Vitals, Topical Decongestants and Normal Saline.

Sedation of the patient is necessary in most cases.

Blood should be arranged for trasnfusion.

If a patient is a known case of HTN, it must be controlled immediately to prevent further blood loss and plasma expanders to be infused.

*patients with posterior nasal packing are usually admitted in the ICU because the PNP may cause oxygen desaturation.

Simplest method for Posterior Nasal Packing?

14 FR Foley's Catheter

Management of Complicated Sinusitis (usually involving the eye and sometimes, the brain also)?

(In order of importance):

History/Examination

Call for assistance from Opthalmology/Neurology

IV antibiotics infusion (Ceftriaxone works best)

Observe for 24 hours, if sympotoms persist then proceed with surgery (Functional Endoscopic Sinus Surgery or External Ethmoidectomy) after a CT scan.

Trauma leading to fracture of the nose, outline the treatment?

History/Examination

X- ray (it has great medicolegal importance)

Analgesics.

Reduction of the fracture ---> ONLY if the patient is brought in within 2 hours of the trama.

*If, however, the patients comes to you 2 hours after the trauma and edema is present then do NOT reduce the fracture then. Give analgesics and send the patient home, call after 7 days (aftet the edema has settled) to reduce the fracture.

Treatment of Septal Hematoma?

Make an incision on one side

Drain the blood

Leave a small drain (to prevent re accumulation)

Pack the nose on both sides (remove after 48 hours)

Start prophylactic Systemic Antobiotics.

Management of post Septoplasty (or any other nasal surgery) Septal Hematoma?

Re-open the already present surgical incision.

Drainage ----> leave the drain in for 1 day ----> Pack the nose

Give an Anti biotic cover.

Treating Septal Abscess?

Incision on the most dependent part of the abcess

Evacuate the pus

(any necrosed cartilage will also be removed)

Place a small drain

Do nasal cavity packing

Send the pus was C/S and till the report comes in keep the patient on broad spectrum antibiotics.

*nasal pack should be removed daily and any pus accumulated should be drained for a few days till the condition subsides.

-Sources: Udairpuwala, Dr. K.I - HOD ENT department ZMUH KDLB, Dr. K.M - Professor of ENT department ZMUH KDLB.