Medical Study Notes For PG Preparation

Types of Long Term Memory

2011-06-23T18:02:00.000+05:30

1. Ericsson and Kintsch (1995) hypothesize that people store not only information but also learning strategies in long-term memory for easy access. This capacity, which Ericsson and Kintsch call long-term working memory, accounts for the extraordinary skills of experts (such as medical diagnosticians) who must match current information with a vast array of patterns held in their long-term memories.

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2. Episodic memory is our memory of personal experiences, a mental movie of things we saw or heard. When you remember what you had for dinner last night or what happened at your high school prom, you are recalling information stored in your long-term episodic memory. Information in episodic memory is stored in the form of images that are organized on the basis of when and where events happened. Episodic memory contains images of experiences organized by when and where they happened. Episodic memories are often difficult to retrieve, because most episodes in our lives are repeated so often that later episodes get mixed up in memory with earlier ones, unless something happens during the episode to make it especially memorable. For example, few people remember what they had for lunch a week ago, much less years ago. However, there is a phenomenon called flashbulb memory in which the occurrence of an important event fixes mainly visual and auditory memories in a person's mind. For example, people who happened to be eating breakfast at the moment they first heard about the attack on the World Trade Center or about Princess Diana's death may well remember that particular meal (and other trivial aspects of the setting) forever.
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3. Long-term semantic memory (or declarative memory) contains the facts and generalized information that we know; concepts, principles, or rules and how to use them; and our problem-solving skills and learning strategies. Information in semantic memory is organized in the form of networks of ideas. It is mentally organized in networks of connected ideas or relationships called schemata (singular: schema). A schema is like an outline, with different concepts or ideas grouped under larger categories. Various aspects of schemata may be related by series of propositions, or relationships.
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4. Procedural memory (Information in procedural memory is stored as a complex of stimulus-response pairings) is the ability to recall how to do something, especially a physical task. This type of memory is apparently stored in a series of stimulus-response pairings. For example, even if you have not ridden a bicycle for a long time, as soon as you get on one, the stimuli begin to evoke responses. When the bike leans to the left (a stimulus), you "instinctively" shift your weight to the right to maintain balance (a response). Other examples of procedural memory include handwriting, typing, and running skills. Neurological studies show that procedural memories are stored in a different part of the brain than are semantic and episodic memories; procedural memories are stored in the cerebellum, whereas semantic and episodic memories are stored in the cerebral cortex.

Colon Cancer - Q & A

2011-01-25T20:07:00.001+05:30

What are the risk factors?
Age > 45 yrs
Lack of dietary fibers & High protein diet (meat)
Alcoholism, Smoking
Cholecystectomy - increased bile acid secretion

Explain briefly the pathology.
Histologically - columnar cell neoplasm
Macroscopically, it's divided into 4 types : annular, tubular, ulcerative and cauliflower type.
Annular type causes predominantly obstructive symptoms, whilst others causes bleeding more often.

Enumerate some common sites involved.
Rectum (most common)
Sigmoid colon
Descending colon
Caecum

Explain the clinical features.

a) Carcinoma of caecum + ascending colon

Patient presents mostly with features of anaemia, weight lost or sometimes abdominal mass. Abdominal pain is not a usual symptoms, however if present, usually is dull aching, or colicky in nature, over the right lower quadrant.

On examination, the patient is usually pale and appears wasted.
If the patient is thin enough, a mass may be visible over the RIF or the right lumbar region, confirmed by palpation, which is usually hard, mobile/fixed.
Percussion over the mass - dull note.
Normal bowel sounds are usually heard.

It's possible that CA caecum can triggers episode of acute appendicitis in such patients. More importantly, there's no difference in the clinical features from the usual ones. Hence, any patient, >45 yrs of age, presented with acute appendicitis, CA caecum should also be suspected. The other differential diagnosis includes :

Caecal diverticulum
Ileocaecal tuberculosis
Crohn's disease

b) Carcinoma involving the left sided colon

The age of the patient is usually >45yrs old.
However, if it involves younger patients (20-30), suspect familial polyposis/or it can even occurs as a complication of long-standing ulcerative colitis.
There's no sexual predilection.
The first complaint is usually altered bowel habits.
There's usually a period of constipation, interpersed in between periods of explosive diarrhoea.
The constipation is obviously caused by obstruction, and diarrhoea is caused by liquefaction of the stools above the obstruction.
Sometimes, the diarrhoea can be worsened by passing mucuos, as when the surrounding colonic mucosa gets inflammed.
Per rectal bleeding is also an important symptom.
The blood is usually dark-plum coloured, sometimes accompanied by some amount of clots.
Especially when the tumour involves sites such as the rectosigmoid junction, it can easily prolapsed into the rectum, causing tenesmus.
Tenesmus is defined as intense desire to evacuate the bowel, but however, nothing passes out (or scanty amount of loose stools) when the patient tried to pass motion.
Commonly associated with sensation of incomplete bowel evacuation.
Lastly, pain is again not a usual feature.
Some amount of dull-aching, or colicky pain may be appreciated over the left lower quadrant of abdomen.
Weight lost usually occurs before anorexia develops.

On examination, patient is wasted.
Mass may be visible/felt over the left iliac fossa or the left lumbar region.
In can be tender when associated with areas of inflammation around the mass.
Indentation of the abdomen at proximal sites may be possible - stool collection
Dull note on percussion over the mass.
Normal bowel sounds are usually heard.

However, if the patient neglects the above symptoms, it can complicates as bowel perforation, that surprisingly, occurs at the caecum instead of the site of malignancy.
Patient can presents with severe generalised abdominal pain, with features of shock.

What are the mode of spreading for CA colon?

1) Direct spread

Longituidinal, transverse or radial.
It usually involves the surrounding bowel wall causing obstruction before invading the adjacent structures.
Sometimes, fistulas are formed when the tumour invades to adjacent structures (vesico-enteric fistula)
Radial spread involving the adjacent organ determines the prognosis.

2) Lymphatic spread

Lymph nodes draining the colon :

L1 -> Nodes located within the vicinity of the colon
L2 -> Right, left colic, mid-colic and ileocolic nodes
L3 -> Nodes originating from the abdominal aorta, close to the superior mesenteric vessels

3) Hematogenous spread

Via the portal system, it spreads to the liver.
Rarely to the skin, lungs, brain

4) Transcoelomic spread

What are the investigations to be done?

Currently, colonscopy is the investigation of choice, provided that the patient is fit enough to undergo bowel preparation.
The advantage is, not only the primary tumour can be clealy visible, but any polyps or other synchronous tumour.
However, it carries a small risk of bowel perforation.

If colonoscopy is contraindicated, Double contrast barium studies can be done.
On abdominal X-ray, we'll be looking for a filling-defect.
Or flexible sigmoidoscopy can be done.

Ultrasound of the liver to look for secondaries.
CT abdomen, thorax as for staging of the malignancy.

Anatomy of the Urinary system

2011-01-25T20:01:00.000+05:30

Upper urinary tract

Both kidneys are situated retroperitoneally on the posterior abdominal wall.
The left kidney is higher than the right kidney.
The diagphram separates the superior poles of both kidneys from the pleura, the 11th and 12th ribs.

Both kidneys are overlying the psoas major, quadratus lumborum, and transversus abdominis from medial to lateral side.

Anteriorly, the right kidney is overlied by the 2nd part of duodenum, ascending colon, and the liver; whilst the left kidney is overlied by the spleen, stomach, tail of pancreas, and the descending colon.

At the hilum, the front-most structure is the renal veins, followed by renal artery and lastly the renal pelvis.

The abdominal ureters runs over the medial edge of the psoas major muscles, which separates it from the transverse process of the vertebras.

Then, it crosses over the bifurcation of the common iliac artery, which separates it from the sacroiliac joint.

Once it gain entry into the pelvis, it runs over the lateral pelvic wall, passing through the ischial spine.

Finally, it runs medially and enters the bladder.

Note the 3 most common site of stone impaction : Pelvi-ureteric junction, Pelvic brim, and the ureteric orifice.

Lower urinary tract

Upto 4 years of age, the bladder is an abdominal organ.

In adults, the bladder is a pelvic organ, well protected by the pelvic bone.

Superiorly, it is separated from the sigmoid colon, and loops of small bowel by a fold of peritoneum. (in females, the body of uterus as well)

Posteriorly, it's related to the seminal vesicles and vas deferens, and the rectum, in the case of male.

Whereas in females, it's related to the supravaginal cervix and vagina.

In males, the neck of bladder is encircled by the prostate, whereas in females, it fuses with the pelvic fascia.

The length of urethra is males is about 20cm, whilst in females, 3-4cm.

In male urethra, it's divided into prostatic urethra, bulbar urethra and penile urethra. The penile urethra is covered by corpus spongiosum.

It opens out to the tip of glans penis lastly.

Renal adenocarcinoma

2011-01-25T19:56:00.002+05:30

Introduction

It's the commonest malignant tumour of the kidney, also known as hypernephroma.
The peak incidence is around the age of 50-70s, male predominance.
The tumour arises from the renal tubules.
Early spread is common in Renal adenocarcinoma :

a) Direct - involving the perinephric tissue, extension into the renal veins, and then the IVC
b) Lymphatic - involving the ipsilateral para-aortic lymph nodes
c) Hematogenous - pelvic bone, vertebras, lungs, etc

Clinical features

1) History suggestive of RCC

Painless hematuria (usually a total hematuria)
General debility (lost of weight, appetite, malaise, weakness)
Bony pain and pathological fractures
Fixed loin pain (pressure over the renal capsule)
Occasionally, a loin mass is felt by the patient

Less common presentations :

a) Pyrexia of unknown origin
b) Varicocele/Bilateral pedal edema

Extension of the tumour involving the left gonadal veins or into the IVC

c) Polycythemia

Excessive production of erythropoeitin from the malignant cells
Facial, skin over palm/soles redness, recurrent venous/arterial thromboses

d) Sudden severe abdominal pain

Haemorrhage into the tumour

e) Hypertension - rare complication

2) On examination

Evidence of recent weight lost
Palpable loin mass, kidney (ballotable), may be tender
Bony tenderness
Evidence of lung metastases

Investigations

Renal ultrasound
CT abdomen, mainly for staging

Treatment

RCC is a radio and chemoresistant tumour, hence the only option is radical nephrectomy, including the perinephric tissue and ipsilateral para-aortic lymph nodes.

Urinary stones

2011-01-25T19:53:00.000+05:30

Introduction

Urinary stones are usually divided into 2 types :

1) Infective

These stones are usually whitish and chalky, and they crumbles easily.

Usually due to impaired drainage of urine, for eg, in cases of prolonged immobilisation or even bladder diverticulum.

Main constituents includes calcium, ammonia, and magnesium phosphate.

2) Metabolic

80% of these stones are calcium-oxalate stones.

Usually due to abnormal concentration of normal constituents (dehydration) Or

presence of abnormal constituents in urine (homocystinuria) Or

excessive amount of normal constituents in urine (hypercalcemia secondary to hyperparathyroidism or hyperuricemia due to gout)

Hence, any recurrent renal/ureteric colic is an indication for such metabolic screening.

Renal and ureteric stones

More common in males, aged in between 30-50 years of age.

The predominant symptom here is pain, which is dependent on the site of the stones.

If it's a renal stone, it causes a dull, sometimes severe fixed renal pain at the loin (region in between the 12th rib and iliac crest)

Once it has entered into the ureter, the pain changes it's nature.

It becomes colicky (in fact, a true colic), radiating from the loin to groin, testes, labia, and even to the tip of penis.

And of course, the pain might be the worst pain ever experience by the patient.

The patient will be jolting around, rolling, in attempt to relieve the pain.

And it's associated with nausea and vomiting.

Macroscopic hematuria is usually not seen.(although evidence of microscopic hematuria more common)

Bear in mind that the first presentation might be in the form of acute pyelonephritis (triad = fever, loin pain, dysuria)

Or some stones can be clinically silent, till it produces significant renal impairment where the patient first presents with features of uraemia.

It's not possible to examine the patient while he/she is having acute pain. Hence, diagnosis is mostly from history.

Bladder stones

Bladder stones are more commonly seen in middle-age and elderly patients.

Most of them are having prostatic diseases.

Common symptoms include increased frequency of micturition, which sometimes can be related to posture.

While standing up, the stones fall onto the bladder trigone.
Hence, there's a stabbing lower abdominal pain or intense desire to micturate.
While lying down supine, symptoms subsided since the stones fall away from the trigone.
There might be intermittent cessation of urinary flow due to the same reason.
Other symptoms includes : hematuria, features of cystitis (suprapubic pain, burning micturition)

Investigations

A pain abdominal X-ray may reveal a radio-opaque lesion seen along the course of ureter.
Usually, an intravenous urogram reveals obstruction caused by the stones.

Midstream urine is sent for urine culture to rule out any infection.
Renal profile is evaluated

Management

First of all, IM diclofenac is to be given to relief pain (pethidine is an alternative)
In case where the stones are <0.5cm in diameter, as it passes out spontaneously, and the patient's condition improves, there's no further interventions required.
However, if there's evidence of hydroureter, hydronephrosis, increasing pain/fever, treatment is required.
Management of choice nowadays is the extracorporal shock wave lithotripsy.

Alternatively, a ureteroscope is inserted to break the stones.
Or in case where the above 2 interventions fails, go for percutaneous nephrolithotomy.

Prostatic diseases

2011-01-25T19:44:00.000+05:30

The two main disease of the prostate :

1) Benign prostatic hyperplasia (BPH)

In brief, what happens is as men ages (>45 yrs), testosterone levels are reduced and the levels can be relatively lower than the estrogen levels.
Hence, estrogenic effects over the prostate causes proliferation, first over the periurethral region.

Note that as the prostate enlarges, it compresses on and elongates the prostatic urethra. Hence, it results in symptoms of bladder outflow obstruction.

Initially, higher pressure is required to force the urine out of the bladder and as it becomes chronic, bladder muscular hypertrophy occurs.

Trabeculum formation occurs and as it saccules, bladder diverticulum forms.

These bladder diverticulum can result in 3 complications of urinary stasis :

Infection, Stones and Tumour

Eventually, these bladder diverticulum causes increased residual urinary volume and hence, back-pressure to the ureter and kidney occurs and hence resulting in hydroureter or even hydronephrosis.

What are the clinical features?

Symptoms usually becomes clinically apparent beyond 50 yrs of age.

1) Frequency

Patient noticed that there's increased frequency of micturition.

This is especially noticable when there's nocturia.

2) Urgency

Patient complains that he can no longer hold his desire to urinate.

There's an urgent need to pass urine once there's desire to urinate.

Sometimes can be associated with incontinence.

3) Hesitancy

Although there's intense desire to micturate, but the waiting time for the urine to start flowing out is delayed.

In other words, there's difficulty in initiating micturation.

4) Poor stream

Yes, there's a weak urinary stream.

5) Terminal dribbling

After cessation of the main stream, usually it ends with terminal dribbling.

As the patient loses his patience, the urine stains the underclothing.

6) Hematuria

Usually an initial or terminal hematuria

7) Uremia

Sometimes, patients can present with features of uremia.

On examination

Look for features of uraemia.

Bladder may be palpable when there's urinary retention.

Per rectal examination :

Remember to ask the patient to pass urine before examining the prostate.

The prostate is diffusely, however asymmetrically enlarged.

Surface, although smooth, can be bosselated since the enlargement is non-uniformed.

The consistency is usually rubbery, firm and homogenous.

Median sulcus of prostate is palpable, and the rectal mucosa overlying the gland is freely mobile.

2) CA prostate

Most common malignancy among men.

Age of presentation is usually around 80s-90s.

Basically, the symptoms are indistinguishable from BPH.

However, in addition to prostatism, other symptoms suggestive of CA prostate includes :

General debility (weight loss, malaise, body weakness, anorexia)

Bony pain (note that the metastatic deposits are osteosclerotic in nature, hence pathological fractures are actually uncommon)

As the tumour invades the adjacent structures, it may cause severe lower abdominal or perineal pain.

On examination -

Bony tenderness

PR examination reveals an asymmetrically enlarged gland, which is distorted and with a irregular, craggy surface.

The consistency is variable/knobbly, as some areas may be stony hard, others may be soft.

The median sulcus may not be palpable, and the rectal mucosa overlying the gland may be fixed.

Investigations

Any patient presents with BPH should be opted for CA prostate screening as well.

a) Full blood count and BUSE

FBC - to look for renal anemia

BUSE - evaluate renal function

b) Serum PSA

Serum PSA of >100ng/ml is significant for distant metastases.

c) Midstream urine collected for urine culture

To rule out urinary tract infections

d) Chest X-ray/X-ray of the spine

For any evidence of metastases

e) Urodynamic studies

f) If malignancy is suspected, prepare a transrectal ultrasonographic guided needle biopsy of the prostate.

Management

For BPH,

1) Symptommatic

If renal function is normal, and CA prostate has been ruled out, initial management should be medical.

For short-term relief of symptoms, start alpha-blockers (terazosin, tamsulosin)

Start finasteride therapy, which inhibits conversion of testosterone to dihydrotestosterone. Hence, this reduces the size of prostate gland.

It will require few months before this drugs start to exhibit it's effect.

2) Acute retention

If patient presents with acute urinary retention :

a) Admit the patient

b) Urinary catheterisation with strict asepsis

c) If not possible, start suprapubic aspiration using a wide cannula

d) Urinary catheter can be kept for 24-48 hrs at most. However, if the urinary symptoms are less, urinary catheter can be removed after 12 hrs. (Prescrbie alfuzosin 10mg/day after that)

3) Chronic retention

First, rule out malignancy and renal function impairment.

If there's renal function impairment leading to electrolyte imbalance (hyperkalemia, hypocalcemia, hyperphosphatemia), correct it first.

Then, only plan for prostectomy

For CA prostate,

1) For indicental focal findings of malignancy :

If the cells are well-differentiated -> wait-and-see

If cells are undifferentiated -> surgery + radiotherapy*

2) Localised malignancy without bony metastases :

Surgery + radiotherapy*

* : only for those with life-expectancy >10yrs

3) With bony metastases

Orchidectomy or start GnRH analogues

Bladder carcinoma

2011-01-25T19:37:00.000+05:30

Pathology

Almost all cases of Bladder carcinomas are originating from the transitional epithelium.

Since, the urothelium is frequently exposed to carcinogens that might be excreted through the urine. Urothelium over the bladder is commonly involved since there's always residual urine.

Occasionally, bladder carcinoma might be squamous cell in nature.

This is usually seen when there's chronic inflammation of the bladder mucosa, caused by stones or schistosomiasis.

Rarely, it presents as adenocarcinoma.

Usually due to local infiltration of tumour from pelvic organs, or bowel.

History and examination

Males are 3 times more likely to have CA bladder than females.

Age of presentation is usually around 60-70s.

Certain occupations are at high risk of developing this malignancy, especially those frequently deals with chemical dyes (Naphthylamine and Benzidine):

Leather workers

Painters or decorators

Paper or rubber manufactures

Dental technicians

Painless and terminal or total hematuria present in about 80% of the cases

Sometimes, patients might be passing out blood clots

Hence, there might be dysuria, or difficulty in micturition

If the residual urine gets infected, there's symptoms of cystitis

If the tumours originating from the ureteric orifice of bladder, loin pain can present

If infiltration had taken place to adjacent structures, lower abdominal pain radiating to the legs might be present

Bear in mind that for patients with recurrent cystitis not responding to treatment, think of CA bladder.

On examination, usually is not very helpful.

Mass may be palpable over the suprapubic area, over even during per rectal examination.

TMN staging of bladder carcinoma

Tis - Carcinoma in situ, means tumour cells are present only over the inner lining

Ta - Non-invasive, papillary tumour

T1 - Invasive, however, yet to involve the bladder musculature

T2a and T2b - Infiltration beyond bladder musculature

T3a and T3b - Infiltration into the fatty tissue around the bladder

T4a and T4b - Invasion into the adjacent organs (prostate, pelvic wall)

Investigation

Intravenous urogram will shows filling defect within bladder :

IF such picture is seen, a retrograde ureteropyelogram is indicated

Then, cystourethrography should be done under general anasthesia for examination of the tumour, and biopsy specimen can be taken.

CT abdomen for staging.

History taking in a case of hematuria

2011-01-25T19:33:00.000+05:30

First of all, the causes of hematuria :

1) Kidney

Glomerular diseases
Polycystic kidney disease
Kidney stones
Trauma (renal biopsy)
Renal adenocarcinoma
Renal TB
Renal vein thrombosis
Embolism

2) Ureter

Ureteric stones
Neoplasm

3) Bladder

Bladder stones
CA bladder
Bladder Trauma
Inflammation (Cystitis, stones, TB)

4) Prostate

Benign Prostatic Hyperplasia
CA prostate

5) Urethra

Urethral trauma
Urethral stones
Neoplasm
Trauma

General causes

Anticoagulants (Warfarin)
Thrombocytopoenia
Sickle cell disease
Malaria
Schistosomiasis
Blood dyscarias (Hemophilia)
Sternous exercises

Red urine

Hemoglobinuria
Myoglobinuria
Beetroot
Senna
Rifampicin
Phenopthalein

History : Important questions!

1) Is there any pain on micturition?
2) Is it :

Painless hematuria? (Renal TB, RCC, CA bladder)
Total hematuria? (suggestive of bleeding from upper urinary tract)
Initial hematuria? (bleeding from lower urinary tract = prostate?urethra?)
Terminal hematuria? (bleeding from prostate?bladder?)

3) Is there family history of renal disease? (Polycystic)
4) Is there any h/o of drug intake? (anticoagulant)
5) Is there any h/o of substance ingestion that might cause red discolouration of urine?
6) Is there travel history? (Malaria/Schistosomiasis)
7) Is there any fixed loin pain? (Renal causes)
8) Is there any colicky loin to groin pain? (Ureteric colic)
9) Any symptoms suggestive of bladder stones? (Frequency, suprapubic pain, etc)
10) Any symptoms of prostatism?
11) Any h/o of trauma? (including renal biopsy)
12) Any h/o of general debility? (malaise, lost of weight, appetite, etc)
13) Any h/o of bleeding disorders?
14) Any h/o of TB in other parts of body? (esp. pulmonary)
15) Any h/o of sternous exercises done recently?
16) Any h/o of dehydration?

Investigations

1) Full blood count
2) ESR
3) Urine microscopy
4) Chest X-ray
5) Coagulation profile (PT and INR)
6) KUB film or IVU (calculus)

Urology - Q & A

2011-01-25T19:23:00.002+05:30

What are the common causes of urinary tract obstruction?

Upper UT obstruction :

Renal, ureteric calculi
Pelvi-ureteric junction obstruction
Retroperitoneal fibrosis (idiopathic, malignancy)
Transitional cell carcinoma
Congenital (Ectopic ureter, ureterocele)
Infections (Schistosomiasis, TB)

Lower UT obstruction :

Urethral causes (stricture, tumour, stone)
Prostate (BPH, CA prostate)
Bladder neck (CA, stones, neurological causes, stricture)

What are the clinical features of acute urinary retention?

Patient usually complains of suprapubic pain, unable to pass urine
Well aware that there's bladder distension
On examination, bladder is palpable with the following features :

An ovoid mass originating from the pelvis
Can't get below the swelling
Tense, tender, smooth surface
Gentle pressure increases desire to micturate
Immobile
Percussion - dull
Positive fluid thrill

Sometimes, the bladder can be extending up to the umbilicus
(in cases of acute on chronic urinary retention)

What are the clinical features of chronic urinary retention?

Bear in mind that there're 2 types of chronic UR :

a) High pressure type

Associated with chronic bladder outflow obstruction
Can progress to hydroureter and hydronephrosis and eventually, obstructive renal failure

b) Low pressure type

Associated with bladder atony
Doesn't progress towards renal failure

Symptom-wise, patient is usually unaware that there's bladder distension
Usually, such condition is painless
However, there's both obstructive and irritative symptoms of micturition (as in BPH)
And, there's overflow incontinence :

The patient can pass an apparently normal volume of urine
However, whenever there's raised intra-abdominal pressure, there's dribbling of urine

On examination :

Bladder is usually palpable, upto the umbilicus
Non-tender, not tense
Gentle pressure may not be associated with any increased desire in micturition
Dull note on percussion, +ve fluid thrill

Briefly discuss about the clinical significance of urodynamic studies

The maximum urinary flow rate can be determined by urodynamic studies.

In men, it's 15-30 ml/sec; in females, it's 20-40 ml/sec.

A graph of urinary flow rate versus time can be plotted, in which different pattern of curves usually indicates different causes of obstruction.

A normal urinary flow : Rises to the peak rapidly, and rapidly drops down to the baseline (as shown above)

In bladder outflow obstruction, there's prolonged rise to poor maximum flow rate and periods of prolonged variability in flow rate

In urethral obstruction, there's a stable, plateu-shaped curve, with prolonged flow rate.

Together with cystometry, the bladder capacity, capacity during desire to micturate, pressure on the detrusor muscle in full bladder, residual urine volume can be determined.

History taking and examination of a swelling

2011-01-25T19:10:00.000+05:30

Some key questions to be asked regarding a swelling (generally)

1. When do you first notice the lump?

REMEMBER, first noticed the lump 3 months ago is not the same as first appeared 3 months ago.

2. How do you notice it?

Below are the 3 commonest answers :

a) It's painful
b) I noticed it accidentally
c) Others told me about it

Generally, if the lump is painful, the commonest aetiology is inflammation.
Most of the patients thought that only painful lumps are cancerous.

3. How does the lump disturbs you?

Basically, the question is asking about the associated symptoms.
It can be pain, discharge, dysphagia, dyspnoea, cosmetically disfiguring, fear of malignancy, etc.

4. Any changes to the lump since you first notice it?

The commonest change is the size.
Whether the lump has increased or decreased in size, or it's size fluctuates.

5. Has the lump ever dissapears before?

Does the lump dissapears when the patient is lying down supine?
or any other activities

6. Do you ever had any other lumps before this?

Asking for multiplicity

7. What do you think is the cause?

Particularly important if there's history of trauma

On examination :

Note the -

a) Position
b) Colour and texture of skin over swelling
c) Size
d) Shape
e) Surface
f) Temperature
g) Tenderness
h) Edge - indistinct/well-defined
i) Composition

Calcified tissues/bone makes the swelling hard
Swelling packed with cells : Firm
Or it might contain fluid (lymph, blood, pus)
Intravascular blood
Gas

j) Consistency

Stony hard - not indentable at all, as hard as bone
Firm - hard, but not as hard as bone
Rubbery - slightly indentable, feels like rubber
Spongy - indentable, but with some resillence
Soft - Squashable, no resillence

k) Fluctuation

Palpate the swelling over 3 planes.
Pressure over the 3rd plane of the swelling usually causes the other 2 planes to buldge out or tensed-up
Positive fluctuation test indicates that the swelling might contains fluid

l) Fluid thrill

Only swelling which contains fluid transmits percussion waves.
Use one of the finger to tap one end of the lump, and feel for the vibration produced at another end, using another finger from another hand.
If the swelling is too large, the percussion wave might be transmitted through the wall.
Hence, one should place a hand at the middle of the swelling to prevent such transmission.

m) Transillumination

If the swelling contains clear fluid, it transilluminate.
It should be done using a small bright light source, in a dark room.
Eg, hydrocele, epididymal cyst

n) Pulsatility

Place one finger of each hand over two ends of the swelling.
If both the fingers are moving upwards and outwards -> expansile (eg, aneurysm)
If both the fingers are moving only upwards (one direction) -> transmitted (a lump overlying an artery)

o) Compressibility

As pressure is applied to the swelling, it's compressed.
But once the pressuring hand is removed, the swelling immediately reappears.

p) Bruits
q) Reducibility

This is different from compressibility.
If the swelling is reducible, it is reduced into another space.
As the pressuring hand is removed, the swelling usually takes some time before reappearing, or will only reappear when there's stimulus, eg cough

r) Relation with surrounding tissue

Is it pinchable from the skin?
When the muscle is tensed,
Does it becomes more prominent, less mobile or less prominent and less easily felt?
When the swelling overlies a nerve/or artery -> not mobile along it's course, but mobile across it's length

s) Any palpable regional lymph nodes?
t) General examination

Short cases - Lumps

2011-01-25T19:02:00.000+05:30

1) Dermoid cyst

Dermoid cyst is a cyst located deep to the skin and lined by the skin.
It forms either due to accident during antenatal development or even following injury, some skin is being implanted into the subcutaneous tissue.
Hence, dermoid cyst can be congenital or accquired.

a) Congenital dermoid cyst

History

May be noticed at birth, or years later when it gradually distends to a noticable size. The common complaints, usually by the parents is cosmetic disfigurement since it's a swelling at the neck and face. Rarely it becomes large enough to cause mechanical disability or affecting the vision.

On examination

Congenital dermoid cyst is usually formed when the skin dermatome fuses.
It's commonly found at the midline trunk, face and neck, outer or inner aspect of eye brow, or behind the ear.
Shape is usually spherical, with diameter of 1-2cm.
Smooth surfaced.
Congenital dermoid cyst over the face is usually soft.
Since it usually doesn't contain clear fluid as it supposed to be (mixture of sebum, sweat and desquamated epithelial cells), it doesn't transilluminate.
It fluctuates and if it's large enough, there's fluid thrill as well.
Skin over the cyst is pinchable.
Non-pulsatile, non-compressible, non-reducible.
Local lymph nodes are not enlarged.

b) Accquired implantational dermoid cyst

History

There's history of old injury, such as deep cut, stab injuries and etc.
These implantational dermoid cyst is usually found over areas susceptible to repeated traumas, eg the fingers.
Hence, it can be painful, or even interferes with gripping and touch.

Examination

Seen over sites liable to repeated trauma - beneath skin of fingers.
Size and shape - Spherical, small with diameter 0.5-1cm
Smoothed surace
Due to it's small size, it's almost impossible to elicit specific signs for cystic swelling, which is fluctuation and fluid thrill.
It's usually hard, and the skin overlying it is usually scarred.
The skin is either tethered deep to the scar or within it.
It's mobile over the deeper structures, which is usually normal.
Commonly confused with sebaceous cyst, but with an old scar and h/o of injury is significant for diagnosis.

2) Subcutaneous Abscess

History

Throbbing pain which steadily worsens, and keeps patient awaken at night.

Patient usually notice a swelling at the site of pain.

May complaints of fever with chills and rigor.

It may rupture and discharging pus out of the skin before they seek medical attention.

The patient may have h/o of diabetes, having debilitating diseases, or even IV drug use.

Examination

Since the buttocks and upper thigh are usual sites of injection, abscess may be formed there. And in IV drug users, over cubital fossa or groin.

Skin over swelling appears red and shinny.

Surface is not definate.

Usually started as a patch of induration, which later as pus collects, a spherical mass is formed.

There's local rise in temperature.

The edge is not palpable since due to the induration and the edema usually fuses with the normal tissue.

It's tender.

Initially it feels hard, when pus started to collect, it becomes soft at the centre and fluctuates.

Skin over swelling is not pinchable.

Regional lymph nodes may be enlarged and tender

3) Sebaceous cyst

Our skin is kept oily and soft by secretions of sebum from sebaceous gland.

The mouth of the sebaceous glands are located at the hair follicles.

Any blockage over these mouth can result in it's distension within it's own secretion and results in formation of sebaceous cyst.

History

Rarely present before adolescence, since it's a slow-growing swelling.

Usually seen in young adults or middle-aged individual.

It's usually detected incidentally by patients as they're combing their hair, when they complained of scratched lump.

It can be infected, where the size suddenly increased rapidly.

Sebum secreted from wide punctum can be later hardened to form a sebaceous horn.

Examination

It's usually present at scalp, back, shoulders, and scrotum. (Never in the palm and soles since there's no sebaceous gland over these areas)

Skin over swelling is normal unless infected.

Shape - spherical, with smooth surface.

Temperature is not raised and is not tender unless it gets infected.

Edge is easily felt, well-defined.

Consistency - hard.

No fluctuations or fluid thrill.

As the swelling increases in size, the point of fixation will be drawn inwards and punctum is formed. Punctum is diagnostic for sebaceous cyst, but however, only one-half of such swelling presents with a punctum.

Skin over swelling is not pinchable.

Local lymph nodes are not palpable.

4) Lipoma

History

Lipoma is a slow-growing swelling, rarely regresses.

Occurs at any age, but relatively uncommon in children.

Not associated with any symptoms, but presents to the doctor usually because they have noticed a lump and wanted to know what it is.

Patients can have multiple lipoma (lipomatosis), usually over the neck and buttocks.

Examination

Common sites of lipoma includes the upper and lower limb, back, buttocks, neck, etc.

Size is variable, shape - hemiovoid, spherical, etc.

On inspection, surface appears smooth. But when the swelling is palpated carefully, especially when firm pressure is applied, it's lobulated and depression in between these lobulations is seen.

Edge is soft, compressible and tends to slip away from examining hands (slip sign)

Composition - solid fat (fat in body temperature is solid instead of fluid)

Consistency - soft

There's pseudofluctuation, since it's consistency is soft. However, one will notice that on gentle pressure,the plane of swelling over palpating fingers are not tense or not buldging out.

There may be pseudo-transillumination.

Skin over swelling is pinchable.

As muscle is tensed, it may either be more prominent or less (it can arise above or beneath the muscle)

Compressible swelling.

No enlargement of regional lymph nodes

An approach to a case of Hematemesis

2011-01-25T18:55:00.000+05:30

Hematemesis means vomiting of blood.
It can be either a frank blood, or altered, coffee-ground coloured blood (altered by digestive enzyme)
The aetiology of hematemesis is usually proximal to the duodenojejunal junction.

Causes

1) Swallowed blood

Due to hemoptysis, epitaxis

2) Oesophageal causes

Ruptured oesophageal varices
Reflux oesophagitis
Esophageal carcinoma

3) Stomach and duodenum

Peptic ulcer disease
Mallory-Weiss disease
Acute gastric erosions
Gastric carcinoma

4) Bleeding disorders

Hemophilia
Thrombocytopoenia
Coagulopathy (due to liver disease)

5) Drugs

NSAIDS
Aspirin
Steroids
Anticoagulants

6) Others

Uremia
Connective tissue disorders

History : Important questions

1) Is there any h/o of epitaxis, hemoptysis?
2) Ask for h/o of chronic liver disease
3) Any retrosternal burning chest pain radiating upwards or heartburn?
4) Any h/o of dysphagia, odynophagia, weight lost?
5) Ask for h/o of peptic ulcer disease
6) Any h/o of consumption of large meal and alcohol?
7) Does the hematemesis preceded by severe bouts of vomiting?
8) Ask for h/o of anaemia
9) Any recent h/o of acute pancreatitis? Any head injuries? (Cushing's ulcer) Or Any h/o of burns? (Curling's ulcer)
10) Any h/o of bleeding disorders? In the family, is there any?
11) Any h/o of drug intake?
12) Ask for symptoms of uraemia

On examination

1) Depends on the severity of bleeding, does the patients appears to be in shock?

Cool extremities
Prolonged capillary filling time
Tachycardia
Hypotension
Reduced skin turgosity
Altered sensorium
Sunken eyeballs
Dry tongue
Reduced urine output

2) Check around the nose - is there any blood?
3) Examine the chest for any cause of hemoptysis
4) Look for pallor
5) Look for signs of chronic liver disease
6) Any epigastric mass, palpable Left SC nodes?
7) Any epigastric tenderness?
8) Any bruises? Any signs of uremia?

Investigations

1) Full blood count, ESR

Hb level, platelet count, any raised ESR? (connective tissue disorders)

2) Liver function test
3) Coagulation profile (PT and INR)
4) BUSE (Renal profile)
5) Oesophagogastroduodenoscopy (OGD)

Rectal bleeding

2011-01-25T18:42:00.000+05:30

Rectal bleeding usually indicates lower GI bleeding (below duodenojejunal junction). Bear in mind that any patient, aged >45 yrs old, with complaints of :

colickly abdominal pain, PR bleeding and changes in bowel habits

Colorectal CA must be considered unless proven otherwise.

Some causes of rectal bleeding

1) Anal cause

a) Haemorrhoids

Piles are very common.
Uncomplicated piles are not painful.

b) Fissure-in-ano

Fissure-in-ano usually causes painful defecation.
The precipitating cause is usually constipation, hence constipation is usually worsened by the patient fear of passing motion, since it's painful.
Pain usually persists for minutes or even hours after defecation.

c) Carcinoma

The history of anal carcinoma is similar to that of Fissure-in-ano.
However, it's usually seen in the elderly.

d) Trauma

History of penetrating injury into the anus.
Sexual abuse? Anal intercourse?

2) Colorectal causes

a) Carcinoma

As mentioned in previous posts

b) Polyps

The history given by patient is usually the same as carcinoma

c) Diverticulitis

The difference between Diverticulitis and Carcinoma :

Duration : Diverticulitis = longer, Carcinoma = shorter
Pain : Diverticulitis = usually painful, Carcinoma = painless (initial)
Bleeding pattern : Diverticulitis = periodic, massive
Carcinoma = usually smaller in amount, persistent
Mass per abdomen : Diverticulitis = tender, Carcinoma = tenderless
Abdominal radiograph : Diverticulitis = diffuse changes, Carcinoma = localised

d) Inflammatory bowel disease

Usually presented as sudden onset of watery diarrhoea, together with brown stools, mucous, and blood. Ulcerative proctitis can presents as tenesmus

e) Ischaemic colitis, angiodysplasia
f) Irradiative colitis

Especially common in patients with pelvic malignancies, due to irradiation

g) Rectal prolapse

Patient usually complaints of something hanging out at his/her back opening besides PR bleeding

3) Small bowel

a) Meckel's diverticulum

Consider this diagnosis in young adults with frequent painless PR bleeding

b) Acute mesenteric infarction

Patient with h/o of cardiac disease (embolism), with complaints of diffuse abdominal pain, PR bleeding, collapse, with signs of shock, etc -> consider this as well

4) Massive Upper GI bleeding

Due to the massive nature of the upper GI bleeding, the intestinal transit is fast, and hence instead of presenting with hematemesis, patient presents with massive PR bleeding, with shock-like features

5) Bleeding disorders
6) Drugs (anticoagulants)
7) Uremic bleeding
8) Infective causes - dysentry

Portal Hypertension

2011-01-25T18:35:00.000+05:30

Anatomy of the portal system :

The portal vein is formed behind the neck of pancreas, at the level of L2, by the superior mesenteric and splenic veins.
It ascends up along the free edge of lesser omentum, behind the common bile duct.
It enters the liver by dividing into two of it's tributaries.
The left and right gastric veins joins to it.
The inferior mesenteric veins drains into the splenic veins.
Portal vein is valveless and hence, if there's a raised in pressure in between the right heart and the splanchnic circulation, portal pressure elevates.
The portal vein carries about 1.5L of blood per minute, originating from :

Small bowel (superior mesenteric vein)
Large bowel (inferior mesenteric vein)
Spleen (Splenic vein)
Gastric vein

Pathophysiology

Normal portal pressure is about 5-10mmHg.
Portal hypertension occurs when the portal pressure elevates beyond 12mmHg.
At this point, the collaterals at sites of porto-systemic anastomosis opens up in order to decompress the elevated pressure in the portal system.
As the portal pressure elevates above 20mmHg, there's a risk of the friable, submucosal esophageal varices to rupture, causing massive hematemesis.

Sites of porto-systemic anastomosis :

1) Between left and short gastric veins (portal) and azygous veins (systemic) at the lower esophagus and stomach

2) Caput medusae : Paraumbilical veins (systemic) and vein within the ligamentum teres (portal)

3) Lower rectum : Superior and middle haemorrhoidal veins (portal) and inferior haemorrhoidal veins (systemic)

4) Perihepatic veins of Sappey : Subdiagphramatic veins (portal) and Veins at the upper surface of right liver lobe (systemic)

5) Retroperitoneal veins of Retzius : Retroperitoneal veins (systemic) and Superior + Inferior mesenteric veins (portal)

Causes :

a) Pre-hepatic Causes :

Portal vein thrombosis - seen in umbilical sepsis (infants)
Splenic vein thrombosis - Complication of pancreatitis, pancreatic tumour

b) Intrahepatic Causes :

i) Pre-sinusoidal :

Schistosomiasis
Primary biliary cirrhosis
Chronic active hepatitis
Sarcoidosis

ii) Sinusoidal :

Cirrhosis
Cytotoxic drugs
Vitamin A intoxication

iii) Post-sinusoidal :

Cirrhosis
Veno-occlusive diseases

c) Post-hepatic causes :

Budd-Chiari's syndrome
Tricuspid regurgitation
Constrictive Pericarditis

Clinical presentation (History and Examination)

Malnutrition
Ascites
Hematemesis and Malena
Encephalopathy
Caput medusae
Splenomegaly
Venous hum heard
Look for signs and symptoms of chronic liver disease

How do you manage these patients?

1) Esophageal varices without prior h/o of bleeding

Medical management is ideal in such cases.
Start Propanolol orally to reduce portal pressure, provided that there's no contraindication against B-blockers.
If contraindication present, isosorbide-5-mononitrate is an alternative.
Studies have shown that B-blockers reduces 45% of the risk of bleeding.

2) Ruptured esophageal varices presented with hematemesis

95% of the cases - originating from the esophageal varices, 5% - gastric origin
First, assess the rate and volume of bleeding :

Take pulse and BP in standing and sitting position
Gain IV ascess - Blood is withdrawn for hematocrit, coagulation profile, LFT and BUSE, blood grouping and cross matching
Provide immediate fluid resuscitation (Crystalloids, colloids, or even blood transfusion)
Insert CVP line - for ease of rapid transfusion later to prevent volume overload

Start Vasopressin IV (Contraindicated in angina) or Somastostatin IV.
Or Octreotide IV (more potent and duration of action is longer)

Usually 3 days later, as the patient's condition has stabilised, start B-blocker to reduce portal pressure and prevent further bleeding.

Plan for endoscopic treatment :

a) Band ligation
b) Sclerotherapy (Sodium Tetradecyl Sulphate - STS)

If the patient is not reponsive to the above measures and still bleeding or endoscopic intervention is not available (district hospitals), a Sangstaken-Blakemore tube can be inserted to prevent bleeding to buy time for deciding what's the next step. (Shoiuld be removed after 48 hrs)

Start oral neomycin (to reduce bowel flora -> less conversion of nitrogenous waste within bowel back to ammonia -> prevent hyperammonemia)
Start lactulose (to reduce bowel transit time)
Repeat every 2 weeks the sclerotherapy/band ligation until all the varices have been treated.

Common Anal Diseases

2011-01-25T18:33:00.000+05:30

Briefly about anatomy of anal canal

The anal canal commences from the level where the rectum passes through the pelvic diaphragm towards the anal verge. The junction in between the anal canal and rectum is the anorectal ring/bundle which can be felt during PR examination.

The internal sphinchter is a circular, non-striated, involuntary muscles innervated by autonomic nerves.

The external sphincter is striated, voluntary muscles innervated by pudendal nerves.

The superior part of external sphincter fuses with the puborectalis muscle to form the anorectal bundle, for maintainance of continence.

The lower part of anal canal is lined by the sensitive squamous cell epithelium

The lymphatic drainage of the lower half of anal canal is drained into the inguinal lymph nodes

Blood supply - superior, middle and inferior rectal vessels.

Haemorrhoids

The anal canal contains 3 anal cushions, which serves as a gas-fluid protective barrier and closes it. When these cushions enlarge, they can prolapse, and when they're damaged, it causes bleeding.

Chronic hemorrhoids produces pile mass, as the processes are compressing on the perianal skin below it, produces external skin tags.

How it cause bleeding?

As these vascular pads becomes haemorrhoids, they assumed into a position closer to the anorectal junction.

During defecation, as the anal canal everts, the stools compressed against the vascular pads, scratching the mucosa over it.

After defecation, the vascular pads are remained scratched, and hence, blood start to trickle down.

If the vascular pads are unable to reduce after the anal sphincter closes, it worsens the bleeding by impairing it's venous return.

Symptoms (History)

Usually seen in individuals > 20 yrs of age. Extremely rare in children.

Bear in mind that uncomplicated piles are not painful.

Hence, it usually causing painless PR bleeding, which can be mild (notice on wiping your ASS after shitting), or can be severe to the extent of splashing all over the lavatory and eventually causing iron deficiency anemia.

Due to mucus discharge from the surface of hemorrhoids, it can cause pruritus ani.

Another important symptom is sensation of prolapse after defecation, or palpable lump. This forms the basis of the classification of piles based on the severity of prolapse :

Grade 1 : Only bleeding, no prolapse

Grade 2 : Prolapse occurs, but reduces spontaneously

Grade 3 : Doesn't reduce spontaneously (reduce manually)

Grade 4 : Irreducible

However, such classification is artificial, since every hemorrhoids prolapsed during defecation, the only way where it leads to bleeding.

Hence, to translate it clinically :

Grade 1

Prolapse occurs during defecation, but reduces back to it's normal position when the anal sphincter closes. Hence, no lump is noticed by the patient.

Grade 2

The prolapse occured during defecation, reduces back spontaneously but slowly.

Only complicated piles, when it strangulates, thrombosed, becomes gangrenous, fibrosed causing pain. Also known as acute hemorrhoidal crisis.

If the patient has any underlying coagulopathy, bleeding disorders, or taking aniticoagulants, piles may bleed massively.

Examination

Don't ever forget that non-prolapsed/thrombosed piles can't be diagnosed by your fingers! It's indistinguishable from normal mucosa.

Hence, a sigmoidoscopy/proctoscopy is very much required.

However, 3rd/4th degree hemorrhoids, since it's visible, you may be able to make a spot diagnosis.

It's a bluish-purplish swelling, with diameter of 1-2cm, with soft mucosal surface, usually non-tender (unless complicated), with mucus-exuding surface.

If it's complicated, it'll be tense, tender, oedematous.

Sigmoidoscopy and proctoscopy is still required to rule out other rectal pathology.

Management

For acute hemorrhoidal crisis, many surgeons thought that surgical intervention at this stage may cause portal pyemia.

But, it's not true -> if early antibiotic coverage is given.

Yet, many surgeons usually wait until the acute phase is over, and then only decide whether hemorrhoidectomy is required.

During acute phase :

Analgesics given.

Apply cold/warm saline bag pressure -> mass usually shrinks after 3-4 days

For 1st-2nd degree haemorrhoids :

Give defecatory advice - only shit when the desire is there (don't simply shit), apply correct shitting position to minimise straining, in addition of stool softerners and bulk forming agents.

Not responsive -> Submucosal injection of 5% phenol in almond oil

Indications of hemorrhoidectomy

1) 3rd-4th degree

2) 2nd degree non-responsive to non-operative management

3) Fibrosed haemorrhoids

Perianal hematoma

It's actually a misnomer, since it's not a true hematoma.

It's caused by thrombosis of a subcutaneous veins within the anal tissue, secondary to injury of venous wall while straining on defecation.

The thrombosis subsequently causing inflammation and edema of the surrounding tissues.

History

Age

Any age, no sexual predilection

Symptoms

Characterised by anal pain, which gradually increases in it's intensity over hours, and subsides after a few days. It causes a continuous discomfort, worsened by sitting, walking, etc.

It is associated with the presence of a lump in the anus, which initially small in size, and gradually enlarges when it becomes more painful.

If the lump ruptures through the skin, or it ulcerates, it can cause PR bleeding.

Since it causes partial opening of the anus, as there's continuous mucus discharge, it results in pruritus ani.

Can be triggered by episodes of straining at stools while defecating.

Signs

The lump can be located anywhere along the anal margin.

The skin over it appears reddish-purplish.

Size is usually small initially (1x1cm), with hemispherical shape, gradually enlarges in size, which becomes polypoidal.

With smooth surface, hard in consistency.

It's tender, but disproportionate to what the patient complaints of.

Not fix to the skin, nor it can be reduced back into the anal canal.

Local/regional lymph nodes are not enlarged.

Fistula in ano

A fistula is a track, lined by squamous epithelium/granulation tissues, connecting two epithelised surface, either in between 2 body cavities, or 1 body cavity - external skin surface.

Hence, fistula in ano is an abnormal, fistulous connection between the rectum or anal canal to the external skin. Usually caused by a ruptured intersphincteric abscess. It has an external opening on the skin, and an internal opening, which can be classified based on it's relative position to the anorectal ring :

High level fistula

Internal opening located above the anorectal ring. As it tracks through the anorectal bundle, it causes incontinence. Different varieties of it includes :

Extra-sphincteric, Trans-sphincteric, Inter-sphincteric

Low level fistula

Internal opening located below anorectal ring. It doesn't cause incontinence.

Different varieties includes :

Trans-sphincteric, Inter-sphincteric, Subcutaneous/Submucosal

Goodsall's rule

According to goodsall's rule, any anterior fistula will have it's internal opening located along a line drawn radially, connecting the external opening to the anus.

Whilst any posterior fistula, regardless of it's position, will have is internal opening, located at the posteior anus, on midline position.

History

Patient may have h/o of perianal abscess, might have been drained or healed.

Commonest symptoms is watery, serous, purulent discharge from the external opening.

They may complaint of bubbling sensation during defecation, as stool passes through the anal canal, it forces mucous discharge from the fistula. This also prevents healing of the fistula.

Periodic throbbing pain can be there as pus accumulates within the tract.

Persistent mucous discharge causing pruritus ani.

Some amount of bleeding might be there. (from external opening)

In your history taking, also ask for symptoms of inflammatory bowel disease, any abdominal upset, systemic upset.

On examination

You'll notice that the discharge can be either serous or pustulous.

The external opening is seen as tufts of granulation tissues or puckered scars.

Rectal examination is usually not painful.

The internal opening is felt as an area of induration or a nodule under the anal mucosa. Most of the time, the tract is palpable.

Look for any other evidence of Anal carcinoma, TB, or IBD.

Confirm your examination findings using sigmoidoscopy/proctoscopy.

If the inguinal nodes are enlarged -> either due to infection of the fistulous tract, or infiltrative anal carcinoma.

Treatment : Fistulotomy, Fistulectomy

Anal fissure

Defined as a longituidinal split in the anal skin.

Acute tear is common, especially when there's excessive straining during defecation (hard stools?), and it usually heals rapidly. But during next defecation, as the stool stretches the anal canal, it causes the split to gape, leading to pain and bleeding. Then, it's so painful that the anal sphincter undergoes spasm.

Hence, a viscious cycle of tear-pain-spasm occurs, and produces further pain. Eventually, as the fissure becomes chronic, fibrosis occurs and a chronic ulcer is produced.

History

This condition can be quite common in children as they frequently passes bulky stools rapidly.

In adults, usually occurs in between 20-40 yrs of age, slightly more common in males. In females, might be seen after delivery.

Severe anal pain on defecation is the chief complaint, which is tearing in character. Persistent, throbbing pain is there minutes or even hours after defecation. It's sometimes so painful that the patient might be apprehensive towards defecation, and ended up accumulating large volume of hard stools within the rectum. This only causes more pain during next defecation.

Since there's spasm of anal sphincter, patient might find it difficult to pass motion. (As for laymen, constipation)

There's streaking of stools with blood, or the patient notices blood while wiping their ass after defecation. As with chronic fissure, there's only mild-bleeding.

In chronic fissures, sometimes there's a sentinel-skin tag palpable at the lower end of the fissure. And due to the hypertrophy of the anal papillae, mucus discharge from the ulcer causing pruritus ani.

Examination

Most anal fissures are located at the posterior midline of anal skin, some at the anterior midline, rarely lateral.

Usually diagnosed by separating the anal skin, and the split is visible.

Rectal examination is usually not possible as it's too painful.

However, if it's not too painful for the patient, anal skin defect can be felt during examination, surrounded by area of induration.

NO proctoscopy/sigmoidoscopy should be done on a conscious patient !!!

Scrotal swelling

2011-01-25T09:56:00.000+05:30

Classifications

1) Congenital
Congenital hydrocele
Congenital indirect inguinal hernia

2) Inflammatory

Cellulitis of scrotal skin - skin appears red, shinny, warm, tender
Pyocele - pus accumulation within tunica vaginalis, fluctuates, non-transilluminant

Orchitis/Epididymo-orchitis/Epididymitis - tender, non-fluctuent swelling
Funiculitis - tender and thickened spermatic cord

3) Neoplastic

There's no benign testicular tumours!

Malignant

Primary : Seminoma, Teratoma, Leydig cell tumour, Sertoli cell tumour, Lymphoma
Secondaries from other sites

4) Others

Hydrocele
Hydatid cyst of morgagni
Epididymal cyst (smooth, uni/multi-locular swelling located behind the testis, brilliantly transilluminate)

Spermatocele (above and behind the upper pole of testis, poorly transilluminate)
Encysted hydrocele of the cord

Varicocele

History taking

1) Onset

Sudden onset of scrotal swelling may be hematocele (with h/o of trauma)
Acute onset can be inflammatory causes (Epididymitis, Orchitis, E-Orchitis)
Insidious - usually hydrocele or testicular tumour

2) Progression

Rapid progression - inflammatory swellings or hemorrhage into a cyst/hydrocele

3) Association with pain

Inflammatory swellings are painful.
Acute epididymo-orchitis must be differentiated from Testicular torsion.

The former, as testis is elevated - pain reduces (increases support on testis)
The latter, as testis is elevated - pain worsens (increases the degree of torsion)

4) Association with fever

Low, moderate, high grade
Intermittent, remittent, continuous
Both acute epididymo-orchitis and scrotal abscess presents with fever

5) Urinary symptoms

A positive h/o of UTI is important for acute epididymo-orchitis
Ask for frequency and dysuria

On examination

1) Inspection

Comment whether one side or both sides are involved
Check whether the swelling extends up to the inguinal region, which can be :

Infantile hydrocele
Inguino-scrotal hernia

Ask the patient to cough, look for expansile cough impulse, which can be :

Hernia, Congenital hydrocele

Inspect the skin over swelling, comment on it's colour and rugosity, whether :

Stretched + shinny -> inflammatory
Stretched + normal rugosity -> Hydrocele, testicular tumours

Inspect whether there's any skin lumps.
Any scars, sinuses?

2) Palpation

Try to get above the swelling, it means that the cord is palpable above the swelling. This is to confirm that it's a pure scrotal swelling.

Comment on the position of testis :

Swelling is anterior to testis -> Hydrocele (but usually hydrocele will be too large for the testis to be separately palpable)
Swelling is attached to the top of testis, cystic -> Hydatid cyst of morgagni
Cystic swelling behind the testis, more towards the upper pole -> Epididymal cyst
Swelling above and behind the upper pole of testis -> Spermatocele
Cystic swelling palpable at the root of scrotum -> Encysted hydrocele of cord

(Can be mistaken as direct inguinal hernia - try pulling the scrotal skin down, it'll descend and becomes less mobile)

Testicular swellings can be either tumour or inflammatory
Varicocele - feels like a bag of worms

Tenderness - for any inflammatory swellings (acute pyocele, hematocele, acute epididymo-orchitis), and sometimes, very tensed cyst

Consistency
Soft - Spermatocele
Cystic - Epididymal cyst
Tense - Hydrocele
Firm - Acute epididymo-orchitis
Hard - Testicular tumours

Palpate the contents of scrotum
Feel for the cord and vas deferens.
The vas deferens will be normal but the cord is thickened - testicular tumour
Both vas deferens and cord is thickened and tender - Acute epididymo-orchitis
Skin not pinchable - testicular tumours infiltrated to skin
Varicocele - bag of worms while patient standing, resolves as he lies down

Cough impulse - Felt in case of hernia, palpable thrill in varicocele

Fluctuation positive - all swelling contains fluid

Transillumination test

3) Examine the inguinal nodes
4) Examine the abdomen

OGDS and Colonoscopy

2011-01-25T09:39:00.000+05:30

As Housemen, you need to know about the indications, preparations, complications

Oesophagogastroduodenoscopy (OGDS)

Indications :

1) For investigation of :

Dyspepsia
Upper GI symptoms not responsive to optimal treatment
Patients >45 yrs with alarmic dyspeptic symptoms, eg :

Chest pain
Odynophagia
Weight loss
Anemia, evidence of GI bleeding
Dysphagia

Dysphagia/Odynophagia
Unexplained iron deficiency anemia
GI bleeding (Acute/Recent/Occult)
Re-evaluation of previous upper GI bleeding
Confirmation of radiologically demonstrated lesion
Suspected portal hypertension
Surveillance of tissue/fluid sampling (Barrett's/Polyposis)

2) Therapeutic interventions

On-going upper GI bleeding (variceal for eg)
Variceal treatment
Removal of selected polyps

Removal of foreign bodies
Dilatation of stenotic lesions
Placement of feeding tube

Palliative treatment for neoplasm

Preparation :

1) Informed consent
2) Patient may need to stop anti-platelet medications (aspirin, clopidogrel) 1 week prior to procedure, and diabetic medication 1 day before procedure
3) Antibiotic prophylaxis for patients with :

Undergoing high-risk endoscopies : Dilatation of stenotic lesions, Variceal bleeding
Previous h/o of infective endocarditis, those with prosthetic heart valves

4) Nil by mouth at least 6 hours prior to procedure
5) Pre-procedural investigations :

FBC, Blood grouping/Cross matching, Coagulation profile, UPT, urinalysis, ECG and chest X ray

6) Sedative given before procedure (diazepam). Hence, ask patient not to come alone or don't drive after procedure.

Contraindications :

Uncooperative patients, Medically unstable patients, risk of perforation is high

Complications : Bleeding, infection, perforation, cardiopulmonary problems

Colonoscopy

Indications :

1) Investigation

Unexplained iron deficiency anemia

Altered bowel habits

Chronic diarrhoea

Inflammatory bowel disease

Lower GI bleeding for patients >40 yrs of age (occult blood is included)

2) Therapeutic

Removal of foreign bodies
Treatment of bleeding
Excision of polyps
Decompression/Megacolon/Volvulus

Preparations :

1) Informed consent
2) Patient may need to stop anti-platelet medications (aspirin, clopidogrel) 1 week prior to procedure, and diabetic medication 1 day before procedure
3) Antibiotic prophylaxis for patients with previous h/o of infective endocarditis, those with prosthetic heart valves
4) 2 days prior to procedure, avoid solid foods, take only food which are easily digestible, eg :

Porridge, Noodles in clear soup, Low Fibre food

5) 1 day prior to procedure, only fluids !

eg, Coffee/Tea without milk, Carbonated drinks (not reddish/purplish), Strained fruit juices

6) Laxatives taken 1 day prior to procedure (tablets bisacodyl)
7) Night before procedure - NIL BY MOUTH
8) Day of procedure - try to empty bowel before procedure
9) Sedative given.

Advanced Trauma Life Support Protocol (ATLS)

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In all trauma cases, the 1st hour is also known as the golden hour, since nearly 30% of death occurs during this period of time.

In the ATLS Protocol, it comprises of :

Primary surveilence - Management of immediately life threatening conditions
Secondary surveilence
Definite management

Primary Surveilence

1) Airway

The first thing to do in any trauma cases is to secure the airway.
Stabilise the cervical spine, using the cervical collar. If not possible, place 2 bags of sand over both sides of patient's head serves the same purpose.

Examine the throat, remove any foreign bodies (dentures), blood clots, or suck out any blood/secretions that might be obstructing the airway.

Next, perform jaw thrust on the patient to straighten the airway.
Try inserting the nasopharyngeal/oropharyngeal airway.
If not possible (airway doesn't open up) -> Endotracheal intubation
One of the ways to check whether patient needs intubation is by looking for the gag reflex. If gag reflex is absent -> INTUBATE

Other indications for ET intubation :

1) Hypoxia (PaO2 <70mmHg, PaCO2 >45mmHg)
2) Seizures
3) Deteriorating consciousness

If ET intubation fails, cricothyroidotomy is the next step.
(Easier to perform compared to tracheostomy).

Locate the cricothyroid membrane, apply horizontal stab incision over it using a scapel.
Insert the scapel handle into the surgically created airway, turn it vertically.
Insert a curved tracheostomy tube.

Deliver high flow oxygen (14-15L/min) through nasal prongs, mask or Endotracheal tube.

2) Breathing

Now that you've secure the airway, next is breathing.
On inspection :

Is there stridor? Wheezing?
Count for the respiratory rate.
Is there central cyanosis over the tongue?
Is there usage of accesory muscles of respiration?
Is there obvious wounds over the chest?
Is there any asymmetry in chest movements? (pneumo/hemothorax)
Is there paradoxical chest movements? (flail chest)

On palpation :

Is there tracheal deviation?
Is there any palpable surgical emphysema (palpable crepitation over neck/chest)?

On percussion and auscultation :

Any dull/hyperresonant note on percussion?
Breathing sound -> is it normal on auscultation?

Now, if there's evidence of pneumothorax, hemothorax, next step is to perform chest drain, as below :

1) Prop the patient in semi-reccumbent position
2) Raise the ipsilateral hand above the head
3) Apply incision on the skin over 5th and 6th ribs, at the anterior axillary line
4) Using forceps, dissect (tunneling) the skin until the pleura is visible
5) Puncture the pleura in upwards direction just above the upper border of the ribs. (To avoid neurovascular bundle of intercostal space)
6) Prepare a catheter, with should be clamped first
7) Insert the catheter, place the other end into a underwater drainage seal bottle. Unclamp the cathter

For simple pneumothorax, tube of size 22-24 F is required.
For massive hemothorax/pneumothorax, tube of size 36-40 F is required.

Connect the patient to a pulse oxymeter.

Tension pneumothorax

A medical emergency - any delay -> death ensues
Symptoms -> Dyspnoea, Tachypnoea, Pleuritic chest pain, collapse
Signs -> Hypotension, Raised JVP, Tracheal deviated to opposite, Hyperresonant percussion note, absent breath sounds

Remember that tension pneumothorax is a clinical diagnosis, where immediate decompression is required by means of needle thoracostomy. (Don't waste time during various investigations)

Needle thoracostomy is performed as follows :

1) Use a wide bore needle with catheter, and puncture the 2nd intercostal space on midclavicular line
2) Rapid gush of air indicates tension pneumothorax
3) Remove the needle, insert the catheter
4) Lastly, connect the other end of catheter into a underwater sealed drainage bottle.

3) Circulation

The goal in circulatory assessment is to determine whether the patient is in shock. Signs indicative of shock :

a) Extremities - cool and clammy
b) Prolonged capillary refilling time (normal is <2 secs)
c) Thready/feeble pulse, with rate >100 bpm
d) Hypotension (systolic BP <90 mmHg)
e) Altered mental status - agitation, confusion, unconscious
f) Abnormal respiration
g) Reduced urine output (normal = 1ml/kg/min)

One should immediately gain IV access, using in case signs of shock is present, using short and wide bore cannula of size 14-16 F
Perform fluid resuscitation -> 2L of Crystalloids given (either normal saline/Ringer lactate/Hartmann's solution)

Don't use dextrose!
Dextrose will be metabolised by our body, rendering the fluid hypotonic, and hence unable to maintained within the vascular compartment.
In other words, they are poor plasma expanders

For patients didn't respond to crystalloids, try colloids (gelufundin)
Any revealed/conceal site of hemorrhage -> compression bandage is applied

If patients condition is not improving or there's major bleed, prepare emergency O blood transfusion.
For males, O +ve blood can be given.
However, for females, only O -ve blood can be given for those within reproductive age group.

Now sent blood for investigations :

FBC, Blood grouping/Cross matching, BUSE, Coagulation profile, ABG

Remember to warm the blood before transfusion to prevent hypothermia. Patient should be covered with blankets as well.

If patient's condition is still not improving, use inotropics (either dobutamine, dopamine, adrenaline, nor-adrenaline)

Cardiac tamponade

In cases of hemopericardium, there's compression over the cardiac chambers, causing obstructive shock, where venous return is impeded.
Becks triad of Obstructive shock = Raised JVP, hypotension, faint/absent heart sounds
Can be diagnosed rapidly using FAST (Focused Abdominal Sonography for Trauma)

First, try needle cardiocentesis.
Usually it's unsuccesful since blood within the pericardium is clotted.
Hence, most of the time, surgical decompression is required.
Mean time waiting for surgery, intropics are given.

Detection of bleeding

Stop all revealed hemorrhage - scalp, skin, nose, etc
For other concealed sites, search over the :

Pleural cavity
Peritoneal cavity
Retroperitoneum
Pericardial cavity
Pelvic cavity
Bone fractures

4) Disability

To assess the neurological impairment on patient.
Start with GCS :

Lowest score 3/15, Highest score 15/15
There are 3 components :

Eye movements

Eye opens spontaneously -> 4
Opens only on verbal stimulus -> 3
Opens only on painful stimulus* -> 2
No response -> 1

*given as sternal rub, squeezing of trapezius

Verbal response

Oriented, conversing -> 5
Disoriented, conversing -> 4
Inappropriate words -> 3
Incoherent words -> 2
No response -> 1
Patient is intubated -> T

Motor response

Moves according to instruction -> 6
Localising pain -> 5
Flexion withdrawal -> 4
Abnormal flexion -> 3
Abnormal extension -> 2
No response -> 1

Next, check for pupillary response towards light.
In case of internal hematoma, initially there'll be constriction, followed by dilatation. If ICP is not reduced, the opposite pupil will be affected as well.

Then, identify any signs of raised ICP.
Finally, examine if there's any signs of 3rd, 4th, 6th nerve palsy or any obvious limb paralysis.

5) Exposure

Cut off the clothes to expose other possible wounds (any lacerations, abrasions, contusions)
Inspect the front and back (for the back, perform log roll)
Any fractures -> splint it

Splint/immobilise any swollen/deformed areas, which can be possibly fractured, to prevent further injury, reduce pain and bleeding.
Any compound fracture, sterile dressing should be applied first.

At the end of primary survey, these should be done :

a) Insertion of Ryle's tube

Insert through nostrils -> known as NG tube
If there's nasal bleeding + h/o of head injury -> fracture of skull base
Hence, Ryle's tube is passed through the mouth -> Orogastric tube (OG tube)

b) Urinary catheterization

Using a self-retaining foley's catheter perform a continuous bladder drainage.
If not possible, perform a suprapubic cystostomy.

Bear in mind that any blood present within the urethral meatus, which may indicate urethral rupture, is one of the contraindication against catheterisation.

(You might convert a partial rupture into a complete rupture by passing the tube!)

Other contraindications includes -> pelvic fracture, perineal injury
Monitor urine output -> to be at least 0.5ml/kg/min

c) Wound

Treat any wound by dressing to prevent contamination
Any bleeding wound should be given compressive dressing

d) Monitor

Monitor patient's vital signs (BP, RR, PR, Temperature), GCS, pupillary response, and Oxygen saturation.

For an unstable patient, connect the patient to an ECG monitor and pulse oxymeter.
Monitor patients vital signs every 15 minutes, until the patient is stabilised for more than 1 hour.

e) Investigations

Blood (as mentioned above)
Urine - FEME
X ray

Lateral view of cervical spine
Chest X ray
Pelvic X ray

History taking and examination of an ulcer

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An ulcer is defined as a break in the continuity of the lining epithelium of tissue. Once an ulcer appears, it's usually noticed by the patients, unless it's painless, or located at non-accessible sites.

History taking

1) When do you notice the ulcer?
Remember that the ulcer might have been present for long before the patient actually notices it. This is usually in case of a neuropathic ulcer.

2) What draws your attention to the ulcer?
Usually is because of pain. Others includes : bleeding, discharge, may be foul-smelling.

3) How does the ulcer disturbs you?
The commonest symptom associated with an ulcer is pain. It might be interfering with eating, walking, defecating, etc

4) Any changes to the ulcer since you've noticed it?
Is there any increase in size, changes in shape, increased discharge, bleeding, or severity of pain?

5) Is there any similar ulcers noticed elsewhere in the body?
Asking for multiplicity.

6) What do you think is the cause of ulcer?
Most of the time the patient will get it right, and the commonest cause is trauma.

Examination

1) Inspect the floor

The floor of an ulcer usually made up of granulation tissues or slough tissues. Sometimes, the underlying structures might been exposed, eg : bones, tendons, etc. Some characteristic contents of the floor are able to provide you a hint to your diagnosis :

Solid-Brown, greyish tissue - Full thickness death of tissue
Slough tissue resembles a yellow-grey wash leather - Syphilitic ulcers
Unhealthy, bluish granulation tissue - Tuberculous ulcers
Poor granulation tissue, with visible bones, tendons, periosteum - Ischaemic ulcer

2) Edge of the ulcer

The edge is the portion in between the floor and margin of an ulcer
There're 5 main types of edges for ulcer :

a) Slopping edge

Usually means the ulcer is superficial/shallow and has a good chance in healing. Healthy granulation tissue usually is pinkish, means it has a good vascularity. A healing epidermis is usually seen extending from the edge, over granulation tissue, either pale/pink in colour (almost transparent)
One example of such ulcer is - venous ulcer

b) Punch-out edge

It means there's rapid death over full thickness of tissue with minimal attempts of the body to repair it. A classical textbook example is the Ulcers seen in tertiary syphilis. Nowadays, ulcers with punch out edges are more commonly seen in neuropathic or peripheral arterial ischaemic ulcers. (PVD)

c) Undermined edge

It means the rate of destruction of the subcutaneous tissue is more rapid than the skin, causing the edge of ulcer to be undermined. Classical example, as it's rarely seen nowadays is tuberculous ulcers. Ulcers with undermined edge is more commonly seen in bedsores, pressure sores as the subcutaneous tissues are more susceptible towards pressure.

d) Everted edges

This means that over the edges of the ulcer, tissues are growing so rapid that it eventually overlaps the overlying skin. This is classically seen in Squamous cell carcinoma.

e) Rolled edges

The tissues over edges are growing slowly, which is usually pale/pink in colour, with telengiectasis seen over the pearly edges. An ulcer with rolled edges is almost diagnostic of a rodent ulcer of Basal cell carcinoma.

3) Depth

Measure the depth of an ulcer by mm

4) Discharge

Discharge from an ulcer can be serous, serosanginous, sanginous, or purulent.

Sometimes, due to the formation of a coagulation discharge scab over an ulcer, it prevents you from examining the entire structure of ulcer (might be missing some of it's features). It's advised that you remove the scab first.

5) Base

Feel the base of the ulcer.

Is it adherent to the underlying structure? (may be bone, periosteum, tendon in cases of osteomyelitis, malignancy)

6) Regional lymph nodes

Please remember to palpate the regional lymph nodes.

It'll be enlarged (and tender) if there's secondary metastatic deposits or any spreading infection.

7) State of the local tissues

Most of the ulcers over the leg is due to poor vascular/nervous supply.

Hence, it's a must that you check for it's vascularity and innervation.

Testicular Tumour

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Just breifly describe about this uncommon, but important condition

First, we'll talk about the anatomy :

Testes are originally retroperitoneal organs, during intra-uterine life.
Just before guys are born, our balls descends down, through the inguinal canal, and enters the scrotal sac at the perineum.

As it descends, it bring along vessels, nerves, lymphatics, and it's primary drainage duct - the vas deferens
All these structures are kept safely within the spermatic cord, which can be described of having :

3 vessels : Cremesteric artery, Artery to Vas, and Testicular artery

3 nerves : Autonomic nerves, Genital branch of genitofemoral nerve, and illioinguinal nerve

3 structures : Lymphatics, Pampiniform venous plexus, and Vas deferens

3 coverings : Cremesteric fascia, Internal and external spermatic fascia

The anterior aspect of our testis is covered by a closed peritoneal sac, known as the tunica vaginalis, formed as a result of the obliteration of processus vaginalis.
The posterolateral aspect, is where a single, long coiled duct located, which is the epididymis.

2 histopathological types of Testicular tumour :

1) Seminoma - arising from the seminiferous tubules
2) Teratoma - it's a malignant germ cell tumour

History taking

1) Age

For teratoma, it's common among young men, around 20-30 yrs of age.
Seminoma may be more common in individuals around 30-40 yrs of age.

2) Symptoms

Now, the usual scenario is : the only symptom is a scrotal swelling
Since this condition is usually painless.
Occasionally, there might be some amount of dragging, or dull-aching pain.
Especially when the swelling increases in it's size, the patient might complaints of heaviness over the affected testicles.

No, It's not painful...

In advanced malignancy, there might be symptoms suggesting of metastasis, eg : breathlessness, lost of appetite/weight, abdominal pain, etc

Examination

1) Inspection

A scrotal swelling is seen, not extending into the inguinal region
No expansile cough impulse seen
Scrotal skin - stretched but with normal rugosity, but in advanced stage, skin may ulcerate/infected
No lumps, no scars, no sinuses

2) Palpation

Able to get above the swelling (pure scrotal swelling la)
Testis is enlarged, swollen
Hard in consistency, non tender
There's loss of testicular sensation, and it's feels heavier than the normal side
Spermatic cord is normal
Skin may not be pinchable if infiltration had taken place
Non-fluctuant, non-transilluminant

3) Please examine the para-aortic and supraclavicular lymph nodes
4) Examine the abdomen -> any hepatomegaly? any masses?
Auscultate the lungs -> any signs of metastases?

Investigation

Here I'll try not to be lengthy la har....

1) Blood : Alpha-fetoprotein, B-HCG, and LDH (Tumour markers)
2) Chest X ray (cannon-ball metastases)
3) CT abdomen for staging
4) Orchidectomy and sent specimen for histological analysis

How do we stage it?

Stage I : Only involve the testis
Stage II : Involving the nodes below diagphram
Stage III : Involving the nodes above diagphram
Stage IV : Hepatic/Pulmonary metastasis

Head injury

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Pathophysiology

90% of the brain metabolism requires blood-borned glucose.
During normal circumstances, the cerebral autoregulation mechanism maintains the cerebral blood flow above 70mmHg, even though the Mean Arterial Pressure (MAP), varies as much as between 50mmHg - 150 mmHg.

*Cerebral perfusion pressure (CPP) = MAP - ICP

However, when there's head injury, this autoregulatory mechanism is disordered. Hence, the CPP fluctuates with MAP, and hence, brain is more vulnerable towards ischaemia.

According to Monro-Kellie's hypothesis, our skull is a rigid structure, and hence will not expand. Intracranial pressure is directly proportionate to the increase in volume of the intracranial structures, including vascular components (blood in vessels), Cerebrospinal fluid (CSF), or the brain tissue itself.

Initially, when there's formation of a space-occupying lesion, the rise in ICP is prevented by transient displacement of venous blood and CSF away from the brain. This decrease in volume compensates for the rise in volume due to formation of space occupying lesion.

But, further rise in the volume of a brain compartment -> even a slightest increase in volume is going to cause a surge in ICP.

Note : ICP can be measured by passing a catheter through the frontal horn of lateral ventricle. In head injuries, ICP is monitored in btw 5-15 mmHg. Bear in mind that normal ICP is <10mmHg

One should never forget that intracranial hypertension is the dreadliest consequence of head injury. The end-stage of raised ICP will be cerebral herniation, which can be :

a) Herniation through the Tentorial hiatus

Tentorial hiatus is an opening at the tentorium cerebelli
As with central herniation, involving the midbrain, features are :

-> Altered consciousness due to midbrain ischaemia
-> Increased muscle tone, and eventually decorticate rigidity
-> Bilateral +ve babinski's sign
-> pupillary constriction, which followed by dilatation, and lastly, becomes static

As for Lateral herniation, involving the temporal lobe (uncus) :

-> Altered consciousness
-> Contralateral hemiparesis, hemiplegia
-> Compression on the 3rd nerve, initially causing ipsilateral pupillary constriction, followed by dilatation, then becomes fixed to light response. Continued rise in ICP results in involvement of the contralateral side of pupil. The sequence of changes in pupillary response is known as Hutchingson's pupil.
-> Others : ptosis, eye deviated inferolaterally

b) Herniation into foramen magnum

If ICP continues to rise, the cerebellar tonsils will herniates into the foramen of magnum, thereby compressing the brainstem and medulla.
This results in Cardiorespiratory collapse, bilateral pinpoint pupil, and flaccid quadriplegia due to lateral corticospinal tract compression.

Note : Signs of Raised intracranial pressure

Papilloedema (swollen optic disc)
Altered level of consciousness
Bradycardia*
Widened pulse pressure*
Decreased systolic BP*
Abnormal breathing pattern (Cheyne's-Stokes/Hyperventilation)

*Cushing's triad
DO NOT PERFORM LUMBAR PUNCTURE IN A PATIENT WITH RAISED ICP!!

Classification of Head injuries

Classification can be made via :

a) Glasgow Coma scale

Minor head injury = No lost of consciousness and GCS is full 15/15
Mild head injury = GCS 14-15 with lost of consciousness
Moderate head injury = GCS 9-13
Severe head injury = GCS 3-8

b) Mechanism of head injury

i) Blunt trauma

Direct injury (Croup injury)
The brain substance collide against a fixed skull.
Usually caused by sudden deceleration/acceleration forces
Resulting in contusion, laceration and intra-cranial bleeding

Indirect injury (Counter-croup)
Injury to the side opposite to the side of trauma.
Hence, subdural/extradural hematoma may be seen opposite to the side blunt trauma

Rotational injury
This occurs in acceleration/deceleration injury.
Such forces creates rotational injury at the junction btw white/grey matter of brain.

ii) Penetrating injury

High velocity - gunshot injuries
Low velocity - stab injuries
In penetrating injury, there's risk of intracranial infection, due to introduction of foreign bodies

c) Morphological

i) Scalp injuries

Cephalhematoma
More commonly seen in infants and children.
Due to collection of blood under the periosteum, resulting in formation of a tense swelling, confined to the margins of underlying bones.
It takes weeks to resolve

Subaponeurotic hematoma
Blood collection in between aponeurosis and pericranium
Formation of a fluctuant swelling involving the whole scalp
Take weeks to resolve as well

Others : Scalp laceration, Scalding (avulsion)

ii) Skull fractures

It can involve the vault or base, and can be open or closed.
In closed fractures, there's no communication with the exterior, so do not expect a nose, ear bleed or leakage of CSF.

For open vault fractures, expect visible brain substance.
For open base fractures :

If it's an anterior cranial fossa fracture -> Raccoon's Sign (periorbital hematoma) + subconjunctival haemorrhage with no posterior limits + CSF rhinnorhoea and nose bleeding

If it's a middle cranial fossa fracture -> Battle's sign (Bruises seen over mastoid and post-auricular region, which forms within 48 hrs) CSF otorrhoea and ear bleeding

Posterior cranial fossa fracture is not easily identified clinically. Most of the time, when there's occipital bone fracture, there'll be a dural venous sinus tear. Usually, there'll be hypertension, bradycardia, changes in respiration and consciousness.

A closed fracutre can be depressed, communited, or linear.

d) Primary/Secondary

Primary head injury occurs during time of impact, it's irreversible, and not treatable, and recovery will largely depends on the type and extent of injury. Remember that neurons once damaged, will not regenerate.
Hence, most of the our treatment will be focusing on secondary head injury.

Causes of Secondary head injury :

1) Hypoxia, with PaO2 <8Kpa
2) Hypotension, with SBP <90mmHg
3) Cerebral perfusion pressure <65mmHg
4) Intracranial pressure >20 mmHg
5) Pyrexia
6) Seizures
7) Metabolic disturbances

e) Intracranial hematomas

Extradural hematoma

More common in children as their dura strips easily to accomodate blood clot
Here, blood collects between the skull and dura mater
Common at the frontal and temporal region, usually associated with local fractures
Middle meningeal artery or dural venous sinuses are teared
Classical presentation : Lucid interval
Others : Headache, vomiting, lost of consciousness, hemiparesis, seizures, signs of raised ICP
Diagnosis is confirmed by CT brain, which reveals a biconvex, lense-shaped hyperdense hematoma.
If the hematoma is stable, conservative treatment suffice.
However, if there's evidence that it's enlarging, perform blurr hole and craniotomy

Subdural hematoma

More common than extradural hematoma
Here, blood collects between the dura mater and arachnoid mater
Clinical features are similar to extradural hematoma
CT brain reveals a cresent shaped hematoma, which concavity directing towards the brain.
Treatment - same

HISTORY TAKING IN HEAD INJURY

1) How did you injure your head?

Basically, you're asking what's the mechanism of injury.
For dangerous mechanisms, such as falling from a height, or high-speed motor vehicle accident, it may be a multisystem injury, including the spine.
For head injury with lost of consciousness, but without any accidental mechanism, consider hypoglycemia, syncope, aneurysmal subarachnoid haemorrhage

2) Ask about the neurological state of patient during and after injury

Is there lost of consciousness?
Is there seizures?
Is the patient able to respond, move, or talk properly after the injury?
Is there antegrade (can't recall what happened after injury) or retrograde (can't recall what happened before injury) amnesia?

3) Then, What's the GCS of the patient during the scene, prior to intubation, and on arrival in hospital?

4) Is there any evidence suggestive of hypoxia, or any cardiovascular instability?

5) Any co-morbid medical illness?

6) Is the patient taking any drugs? (esp antiplatelets or anticoagulants)

7) Any ilicit drung intake or alcohol consumption

Extradural hematoma

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This refers to collection of blood in between the skull and dura mater.
More commonly seen in younger patients (children, adolescence)
Extradural hematoma is always associated with skull fractures, most frequently, the temporal bone. (since pterion is the thinnest part of skull, involvement of this area causes tearing of the middle meningeal artery)
Of course, involvement of the posterior fossa and frontal bone is also possible.
However, the hematoma is not always arterial in origin, it may be due to a tear to the dural venous sinuses as well.

Classical presentation of extradural hematoma is : (<1/3 of the cases)

Lucid interval, where after initial injury, patient is conscious, alert, oriented, and only complaints of headache. Minutes or hours later, the condition worsens, with deterioration of consciousness, contralateral hemiparesis/plegia, and ipsilateral pupillary dilatation.

Early diagnosis and treatment of subdural hematoma is VITAL.
CT brain is confirmatory, where it'll appears as a lentiform, biconvex, or lense-shaped hyperdense mass in between the skull and brain, with or without midline shift.

After diagnosis is confirmed, surgical evacuation of the hematoma is required, where craniotomy is performed.

Acute subdural hematoma (ASH)

This is actually more common, with poorer prognosis, higher mortality rate as compared to extradural hematoma.
It refers to blood collection in between the dura and arachnoid mater.
ASH is almost always associated with a primary brain injury.
Most of the time at presentation, the patient has impaired consciousness, which rapidly deteriorates depending on the size of the hematoma.

Again, CT brain is diagnostic.
It'll appears as a crescent shaped, more diffuse (with concavity towards the brain), hyperdense mass in between the brain and skull.

Treatment - surgical evacuation by craniotomy

Chronic subdural hematoma (CSH)

CSH often seen in elderly patients, who is on anti-platelets or anti-coagulants. It is believed to be due to tearing of the bridging veins, which causes formation of clinically inapparent, small ASH. Later, as it breaks down and the volume expands, it becomes symptommatic.

Mostly, patients presents with headache, focal neurological deficit, impaired cognition, seizures, etc (hence, one of the d/d of CVA)

CT brain intepretation :

Acute blood (0-10 days) = hyperdense
Subacute blood (10 days - 2 weeks) = isodense
Chronic blood (>2weeks) = hypodense

Treatment = creating a blurr hole and evacuate the hematoma

Management of mild head injury (GCS 14-15)

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Most of the occasions, patients with mild head injury, after history and examination, and a period of observation, will be allowed to be discharge after following criterias met:

Battle's sign

a) Full GCS score (15/15)
b) No focal neurological deficits
c) Accompanied by a responsible adult
d) Not under influence of any drugs/alcohol
e) Verbal/Written advice about the injury given

Racoon's Sign

Statement e) means : Advice regarding any worsening of symptoms, such as persistent headahce not relieved by analgesia, severe vomiting, blurring of vision, diplopia, weakness/numbness of limbs have been given verbally or written.

Sometimes, for patients with mild head injury, decision of whether to perform CT brain or not can be a big headahce. However, here are the NICE guidelines regarding indications of CT brain in patients with mild head injury :

a) GCS is <13 at any point
b) GCS is 13-14 at 2 hours time
c) Evidence of focal neurological deficit
d) Suspicion of open, comminuted, depressed, or basal skull fracture
e) Vomiting > 1 episode
f) Seizures

Urgent indication

a) Age > 65 years old
b) Evidence of coagulopathy (liver disease, blood dyscarias, warfarin, anti-platelet medications)
c) Dangerous mechanism of head injury (CT within 8 hrs)
d) Antegrade amnesia > 30 mins (CT within 8 hrs)

Management of moderate/severe head injury

First of all, resuscitation and primary survery.
After stabilising cervical spine at 3 fixation point, start primary surveying.
Remember that normalising the patient's oxygenation and circulation is more important than getting a CT done! This is to prevent secondary brain injury

After primary survey, you've made a diagnosis of moderate/severe head injury, the next step is CT brain, to detect any intracranial hematoma, or any skull fractures, soft tissue injuries, or any mild intracerebral contusion.
For intubated patients, it's recommended that you've asked for CT cervical spine.

Before ariving at the hospital, some conservative management can be given for raised ICP, which includes :

a) Reversed tredelenburg : Raised head upto 20-30 degrees
b) Check if the cervical collar is too tight (may obstruct venous drainage from brain)
c) If there's pupillary dilatation (may be due to acute raised ICP), 0.5mg/kg 20% IV mannitol can be given.

Medical management of severe head injury

Severe head injury is preferably managed in a neurointensive care unit.
ICP can be monitored by passing a catheter into the frontal horn of the lateral ventricle (2 finger breadth from the blurred hole, behind the hairline)
Raise the patient's head for about 20-30 degrees

Protect the patient's airway!
For those with traumatic brain injury and coma, they are more prone to aspiration.
Preferably intubate the patient, and provide high flow oxygen. (Prevent hypoxia)

Make sure that the cervical collar is not too tight.

Cerebral vasculatures are very sensitive to the PCo2 level. When there's a rise in PCo2 level, the cerebral vasculatures dilates, and elevates the ICP. In contrast, when there's a fall in PCo2 level, cerebral vasculature constricts.

Hence, you must try to maintain the PCo2 level in between 4.5-5kPa.
Some experienced anesthetist may induce hyperventilation in patients to cause temporary reduction in ICP by reducing the PCo2 level.

Sedative given, either with or without muscle relaxant.
Mannitol/Frusemide given to reduce cerebral edema.
Patient is prone for hyponatremia or other electrolyte imbalance -> correct it
Avoid pyrexia, as it'll cause undesirable increase in the brain metabolic activity.
Barbiturates eg: thiopentone sodium is given to reduce ICP and brain metabolic rate.
Prophylactic anticonvulsant given.

A case of Acute testicular pain

2011-01-25T09:06:00.000+05:30

History

We have a 16 years old male here presented to the ER complaining of sudden onset of right testicular pain. The pain woke him up from his sleep and has persisted over the last 3 hrs. His mother says that he has vomited once. His previous medical history includes a similar event a year ago, but on that occasion the pain subsided quickly. He is an asthmatic and uses a salbutamol inhaler.

Only with h/o, what's your differential diagnosis?

Testicular torsion?
Acute epididymo-orchitis?
Torsion of appendix testis?
Infected hydrocele?
Strangulated hernia?
Testicular rupture?
Haemorrhage into a tumour?

On examination

The left hemi-scrotum feels normal but the right side is acutely swollen and tender on palpation. The testicle is elevated when compared to the other side and has an abnormal horizontal lie. The abdomen is soft, non tender, with intact hernial orifices. Vitals are stable, cremesteric reflex is absent.

So, what's your provisional diagnosis?

In this case, testicular torsion should be ruled out unless proven otherwise. Points towards diagnosis of testicular torsion :

1) Age (testicular torsion is common in age group of 10-25 yrs old)
2) Elevated, tender right testicle
3) Abnormal horizontal lie (risk factor for torsion)
4) Cremesteric reflex is absent (bear in mind that presence of this reflex doesn't rule out testicular torsion!)

If doppler's ultrasound is immediately available, a results showing interrupted blood supply to the testis is diagnostic.
However, if the diagnosis is in doubt, PLS peform surgical exploration to confirm the diagnosis. If not, he CAN SUE YOU BECOZ you've caused him to lose his precious balls.

Remember, you've only 4-6 hours (starting from the time of onset of pain) to salvage the balls.
However, if the patient presented within the first hour after onset of pain, it's sometimes possible to untwist the cord manually, which if succesful, the affected testicle is out of danger and surgery can be planned later.

And, surgical correction is bilateral, since congenital defects often involves both sides.

Thoracic Trauma

2011-01-25T09:04:00.000+05:30

Introduction

Thoracic trauma accounts for about 25% of all cases of trauma.
Most of the thoracic injuries are life theratening, where the commonest cause of morbidity and mortality is hypoxia and haemorrhage.
However, ironically upto 80% of the cases can be managed conservatively.
The key to succesful management here is early physiological resuscitation and accurate diagnosis.

Investigations

An approach towards chest injuries is the same as any other injuries in primary and secondary survey, as noted by the Advanced Trauma Life Support Protocol (ATLS). History and examination will be important, and probably the most useful tool is a chest radiography.

In an unstable patient, chest radiography can be done first, provided that it didn't interfere with the process of resuscitation. An ultrasound can give useful information about the presence of hematoma together with a contusion or just contusion alone. Chest drain can be both diagnostic and therapeutic, where the benefits outweights the risks.

Some pitfalls during investigations :

a) Failed to identify tracheal shift
b) Failed to pass NG tube due to failure to recognise diagphramatic rupture
c) During hemothorax, must auscultate both anterior and posterior chest
d) Failed to resuscitate the patient first before investigations are done (both should be done hand in hand)

Nowadays, CT scan made an important role in the management of chest injuries.
Not only it can provide details about ribs and verterbral fractures, it can pick up contusions, hematomas, pneumothoraces easily. In penetrating injuries, eg gunshot wounds, CT can even trace the track of penetration through the thorax. Though aortogram is the 'gold standard' in diagnosing disruption of thoracic aorta, CT scan yields the similar results.

Immediately life threatening chest injuries :

a) Airway obstruction

The commonest cause of early preventable death in a case of thoracic injury is airway obstruction, which blood, clots, secretions, dentures, teeth or even tongue can be a source of obstruction. Rapid removal usually relieves the obstruction.

Examples of injuries potentially causing airway obstruction :

a) Expanding neck hematomas
b) Bilateral mandibular fractures

Both a and b causing pharyngeal deviation and tracheal compression

c) Laryngeal injury with thyroid/cricoid cartilage fracture, and other tracheal injuries

What need to be done immediately is endotracheal intubation, as early as possible.
Since most of these conditions are insidious and yet progressive, and delay will render increased difficulty in inserting the ET tube.

b) Tension pneumothorax

Tension pneumothorax occurs when "one-way" valve is created in such a way that air is collected within the pleural cavity, without any means of escape. The source of air leakage can be originating from the chest wall or lung parenchyma. This results in significant compression over the affected lung, obstruction of the great veins compromising the venous return, mediastinal shift and eventually, compression of the opposite lung.

Common causes includes, penetrating chest injuries, blunt chest trauma with parenchymal injury, iatrogenic causes includes a central subclavian venepuncture or mechanical positive pressure ventilation that has gone wrong.

The clinical presentation is dramatic, with a panicky patient, complaints of dyspnoea, and with distended neck veins. Clinical signs : Tracheal shift to the opposite side (late presentation), diminished lung expansion over affected side, hyperresonant note on percussion, absence breath sounds.

Tension pneumothorax is a clinical diagnosis, NEVER EVER proceed to radiological investigations first.
If clinical diagnosis is establish, one should use a large bore needle, puncture the anterior chest and the 2nd intercostal space, along the midclavicular line. This is followed by inserting a chest tube over the 5th intercostal space at the anterior axillary line.

c) Pericardial tamponade

In a case of patient with shock and distended vein, pericardial tamponade must be differentiated from tension pneumothorax. Pericardial tamponade is usually caused by penetrating chest injuries, and due to the non-distensible feature of the pericardial sac, even accumulation of small volume of blood is going to cause significant mechanical obstruction which renders cardiac pump failure.

The typical presentation will be : Features of hemorrhagic shock, Raised JVP and CVP, muffled heart sounds. Some pitfalls of these presentation must be remembered :

i) In case where there's active bleeding from a site distant to site of pathology, the neck veins are not distended.

ii) In case where the patient is having circulatory collapse, CVP will not be raised

To buy time for preparing the patient for definite operative management, which is left thoracotomy and sternotomy, a needle pericardiocentesis and resuscitation can be done. Needle pericardiocentesis is NOT a substitute for surgical management, and is done with ECG guidance (related with high incidence of iatrogenic myocardial injury)

d) Open pneumothorax

This means an opening chest wound is present, where the size of the defect is > 3cm.
Every breath that is inhaled, more air will be accumulated within the affected hemithorax.
This eventually causes significant hypoventilation, and eventually hypoxia.
The signs and symptoms are directly proportional to the size of the defect.
Initial management includes covering the chest wound is a sterile plastic occlusive dressing, which is only adhered at 3 sites, creating a flutter-wave valve, while suction is continued, where the tube is connected to an underwater seal drainage bottle.
Remember, no 'sucking' chest wound should be covered completely before a controlled drainage is established..
Definite management : pulmonary debridement and closure of the wound.

Some pit falls regarding this conditions :

For adults, a larger tube is required (>28 FG in size)
Some patients may require 2 chest drains
In case where patient's condition doesn't improve despite adequate drainage, try reducing the pressure within the seal drainage bottle to 5cm H20.
Early mobilisation and physiotherapy is required

e) Massive hemothorax

Defined by : initial blood collection by chest drain of > 1500 ml or in on-going hemorrhage, > 200-300 ml/h of blood collected over a period of 2-3 hours.

Massive hemothorax usually occurs due to blunt injuries, rupturing the intercostal and internal mammary vessels. Blood is hence collected within the affected hemithorax, causing significant respiratory distress. It's recognised by signs of haemorrhagic shock, flat neck veins, diminished expansion, dullness on percussion, absence of breath sounds.

Initial management of massive hemothorax includes chest drain, resuscitation and sometimes, intubation. Blood from the pleural cavity must be drained as rapid and as complete as possible, in order to prevent possibility of empyema and later, fibrothorax.

Pit falls regarding massive hemothorax :

1) One must examine both anterior and posterior chest when the patient is lying in a supine position, since there's a chance where the affected lung 'floats' within the BLOODY thoracic cavity.
If you only auscultate the anterior chest - it'll be normal

2) Even after draining out about 500ml of blood, dullness still persist and radio-opacity still present -> emergency thoracotomy

f) Flial chest

Flial chest is defined as a loss of bony continuity of a chest wall segment with the rest of thoracic cage, caused by a blunt trauma, which occurs when there's :

i) 3 or more rib fractures
ii) occurs in more than 2-3 places

Flial chest is a clinical diagnosis, not by chest radiography.
It's done by observing few respiratory cycles, where the flial segment will be drawn inwards during inspiration.

Causes of hypoxia in flial chest : voluntary splinting due to pain, pulmonary contusion, defect in the mechanical movement of the rib cage

Initial management : opiate analgesics, oxygen support. If a chest drain is present, intrapleural local analgesia can be given. Ventilation is reseved for patients with respiratory failure despite optimal treatment given. Surgical fixation is done in severe thoracic injury or in cases where pulmonary contusion is present.