learn anesthesia and have fun

2016-02-17T12:30:00.001+03:00

Hypertensive Disorders in Pregnancy( a quick review)

Hypertensive disorders of pregnancy can be classified as:

1. Gestational hypertension (formerly PIH or transient hypertension)

2. Pre-eclampsia and eclampsia

3. Pre-eclampsia superimposed on chronic hypertension

4. Chronic hypertension.

Gestational hypertension: It is said to be present when BP > 140/90 mm Hg for first time during pregnancy after 20 weeks, but no proteinuria. This is transient hypertension and blood pressure returns to normal by 12 weeks postpartum.

Pre-eclampsia: It is defined as new hypertension presenting after 20 weeks with significant proteinuria [more than 300 mg per 24 hours, or persistent 30 mg/dL (1+ on dipstick)] in random urine samples.

Chronic hypertension: BP > 140/90 mm Hg before pregnancy or diagnosed before 20 weeks gestation or hypertension first diagnosed after 20 weeks of gestation and persistent after 12 weeks postpartum.

Superimposed pre-eclampsia (on chronic hypertension): All chronic hypertensive disorders regardless of their cause predispose to development of superimposed pre-eclampsia or eclampsia. Pre-eclampsia is accompanied by proteinuria.

The pathogenesis of pre-eclampsia

Theories for development of pre-eclampsia:

1. Increased pressor responses: Women with PIH have been found to have increased vascular sensitivity to pressors.

2. Prostaglandins: In PIH, there is decreased prostacyclin production and increased thromboxane A2; resulting in vasoconstriction and sensitivity to infused Angiotensin II.

3.Nitric oxide Decreased levels are found in PIH patients.

4. Vascular endothelial growth factor (VEGF):

VEGF has been reported to be increased in serum from women with pre-eclampsia.

5. Genetic predisposition

6. Immunological factors: PIH is probably an immune response to antigenic sites on placenta.

7.Inflammatory factors: Pre-eclampsia is considered a disease due to extreme state of activated leukocytes in the maternal circulation.

the prediction of pre-eclampsia:

A variety of biochemical and biophysical markers have been proposed for the purpose of predicting the development of pre-eclampsia later in pregnancy.

Rollover test: The patient is asked to assume supine position after lying laterally recumbent. A positive test is an elevation of 20 mm Hg or more in systolic blood pressure. This test has a very good correlation with the angiotensin sensitivity test.

2. Elevated uric acid levels > 5.9 mg/dL.

3. Calcium metabolism: Hypocalciuria seen with pre-eclampsia.

4. Angiotensin II infusion test: It is difficult to perform and hence not used in routine clinical practice.

5. Decreased urinary Kallikreins excretion: Might precede development of pre-eclampsia.

6. Increased cellular plasma fibronectin: these generally precede the development of pre-eclampsia.

7. Coagulation activation: Thrombocytopenia and abnormal platelet aggregation appear to be an integral feature of pre-eclampsia. Excessive platelet activation has been linked to maternal vasoconstriction, endothelial cell injury, placental infarction (atherosis and fetal growth restriction) and transient renal dysfunction. Thromboxane A2 is released promoting vasospasm, further platelet aggregation and endothelial cell injury.

8. Immunological factors: Levels of TNF-α, growth factors and interleukins increased.

9. Placental peptides: Increased corticotropin—releasing hormone, Activin A and Inhibin A.

Risk Factors for Pre-eclampsia

As per NICE guidelines 2010, the following have been described to be risk factors for pre-eclampsia.

High risk factors (any one)

1. Hypertension during last pregnancy

2. Chronic renal disease

3. Autoimmune disorders like SLE

4. Diabetes

5. Chronic hypertension.

Moderate risk factors (more than one)

First pregnancy

Age 40 years or older

Pregnancy interval of more than 10 years

Body mass index (BMI) of 35 kg/m2 or more at first visit

Family history of pre-eclampsia

Multiple pregnancies.

Pathological Manifestations of Pre-eclampsia

1. Cardiovascular changes are basically related to increase in cardiac afterload due to hypertension.

2. Hematological changes: Thrombocytopenia (defined as platelet count less than 1,00,000/mm3) is likely due to platelet activation and consumption and reduced platelet production. The other changes include: microangiopathic hemolysis (due to intense vasospasm), decreased clotting factors, increased erythrocyte destruction, increased fibrin degradation products and deficiency of antithrombin III.

3. Endocrine changes: Increase in deoxycorticosterone in third trimester due to conversion from plasma progesterone causes retention of sodium. Sodium retention leads to inhibition of juxtaglomerular apparatus resulting in decreased plasma levels of renin, angiotensin II and aldosterone as compared with normotensive pregnancy.

4. Fluid and electrolyte changes: In pre-eclampsia there is decreased plasma oncotic pressure, which leads to

increased extracellular fluid with associated decrease in intravascular volume.

5. Kidney: Oliguria is a result of reduced renal perfusion and glomerular filtration. Plasma uric acid and serum creatinine are elevated. There is proteinuria > 300 mg per 24 hours or more than 1 + on urinary dipstick test. Acute renal failure and renal cortical necrosis may develop in severe cases.

6. Liver: Pre-eclampsia is often associated with increased liver enzymes. Epigastric and right hypochondriac pain when present; is due to periportal hemorrhagic necrosis, which causes hepatic rupture or subcapsular hematoma.

7. HELLP syndrome: Triad of Hemolysis, elevated liver enzymes and low platelets.

8. Nervous system: Cerebral edema, hyperemia, focal thrombosis and hemorrhage may be present in severe cases. Retinal artery vasospasm may cause visual disturbances. Increased cerebral perfusion pressure may cause severe headaches.

9. Uterus and placenta: Incomplete trophoblastic invasion of spiral arteries causes reduction in diameter of vessels as compared to normal. In addition, vasospasm decreases placental perfusion leading to Intra Uterine Growth Retardation (IUGR).

Conditions mandate immediate delivery

Severe hypertension that persists after 24 to 48 hours of treatment

Progressive thrombocytopenia

Liver dysfunction

Progressive renal dysfunction

Premonitory signs of eclampsia

Evidence of fetal jeopardy

Persistent headache or other neurologic sequelae of pre-eclampsia.

Adverse Effects of Painful Labor

Painful labor causes maternal hyperventilation. The resulting alkalosis shifts the oxyhemoglobin dissociation curve to the left in the mother. This results in increased binding of maternal hemoglobin to oxygen and reduced oxygen delivery to the fetus.

Hyperventilation at the time of uterine contractions is followed by hypoventilation in between the contractions. This can result in fetal hypoxemia.

Catecholamine release in response to labor pain causes reduction in uterine blood flow.

The hypertensive response to sympathetic stimulation is detrimental in the hypertensive mother.

Sympathetic stimulation causes maternal acidosis because of lactic acid production from skeletal muscle activity and free fatty acid activation. Lactic acidosis can cause incoordinate uterine action and prolonged labor.

Techniques of Labor Analgesia

Nonpharmacological Techniques

Psychoprophylactic approach of Lamaze

Leboyer’s technique: In this method baby is allowed to be born in a quiet dimly lit room, with minimal noise to reduce the trauma and stress for the newborn.

Transcutaneous electrical nerve stimulation (TENS).

Aromatherapy.

Hypnosis.

Acupuncture.

Reflexology.

Pharmacological techniques

Entonox: This is a 50% mixture of nitrous oxide in oxygen. It is delivered to the patient via a demand valve through a low resistance breathing system from the cylinder after pressure reduction.

Sevox: Patient-controlled inhalation analgesia.

It is used in the concentration of 0.8% with oxygen and needs specialized equipment.

Opioids:

Pethidine

is used in the dose of 100 to 150 mg IM. Pethidine 25 mg IV and Nalbuphine 10 mg IV are also used.

Epidural analgesia: This is the most effective method of producing pain relief in labor.

Subarachnoid block: This is not a suitable technique to produce pain relief during labor as the duration of block is too short. CSE is preferred as it has the advantage of immediate pain relief and prolongation of action by using the epidural catheter.

Techniques of labor analgesia.

1. Informed consent is obtained, and the obstetrician consulted.

2. Monitoring includes:

a. Blood pressure every 1–2 min for 15 minutes after giving a bolus of LA.

b. Continuous maternal heart rate during procedure.

c. Fetal heart rate monitoring.

3. Hydration with 500–1000 mL of RL (co load).

4. The woman assumes a lateral decubitus or sitting position.

5. The epidural space is identified with a loss of resistance technique.

6. The epidural catheter is threaded 3 cm into the epidural space.

7. A test dose of 3 mL of 1.5% lidocaine or 0.25% bupivacaine with 1:200,000 epinephrine is injected as test dose. There are reservations to use epinephrine in the test dose. Another method for ruling out intravascular placement is using 100 μg of fentanyl epidurally and watch for drowsiness and euphoria, which is seen within 5–10 minutes in case the catheter is accidently placed in the intravascular space (sensitivity 92.4% and specificity 92%).

8. If test dose is negative, a bolus dose of 0.065–0.125% bupivacaine is injected to achieve a cephalad sensory level.

9. After 15–20 minutes, the block is assessed using loss of sensation to cold or pinprick. If no block is evident, the catheter should be reinserted. If the block is asymmetrical, the epidural catheter should be withdrawn 0.5–1.0 cm and an additional 3–5 mL of bupivacaine injected. If the block remains inadequate, the catheter should be reinserted.

10. Caval compression should be strictly avoided throughout labor, as the hypotension due to epidural may be aggravated due to aortocaval compression. The patient has to be nursed in sitting or lateral position.

11. Maternal blood pressure is recorded every 5–15 minutes. The fetal heart rate is monitored continuously.

12. The level of analgesia and intensity of motor block should be assessed hourly.

Drugs:

Bupivacaine is the local anesthetic of choice.

Bupivacaine 1–2.5 mg with fentanyl 10–25 microgram has a rapid onset and lasts for 90–120 minutes. This is followed by epidural infusion.

Signs of impending eclampsia

Headache

Visual disturbance, such as blurring or flashing before the eyes

Epigastric pain

Oliguria

Vomiting

Sudden swelling of the face, hands or feet.

It has been proved that magnesium sulfate is superior to phenytoin in preventing eclamptic seizures.

loading dose of 4 g should be given intravenously over 5 minutes, followed by an infusion of 1 g/hour maintained for 24 hours. Recurrent seizures should be treated with a further dose of 2–4 g given over 5 minutes. Measure Mg level at 4–6 h and adjust infusion to maintain levels between 4–7 mEq/L. MgSO4 is discontinued 24 h after delivery.

Monitoring and management of MgSO4 toxicity

When a patient is started on MgSO4 it is necessary to monitor:

Patellar reflex (disappears when plasma magnesium level reaches 10 mEq/L; warning impending Mg toxicity)

Rate and depth of respiration (depressed at level above 10 mq/L, respiratory paralysis and arrest occurs above 12 mEq/L)

Urine output (Mg is cleared totally by renal excretion, when there is renal insufficiency, plasma magnesium level needs to be checked periodically and dosage adjusted accordingly).

Table 12.2 Plasma magnesium levels in mEq/L and clinical effects

Sr magnesium (mEq/L) Clinical manifestation1

.5 – 2.0 Normal plasma level

4 – 8 Therapeutic level

5 – 10 ECG changes (wide QRS, > PQ )loss of deep tendon reflexes, SA and AV nodal block, Respiratory paralysis

25 Cardiac arrest

Treatment

Withhold MgSO4.

Administer Calcium gluconate, 1 g intravenously.

For severe respiratory depression and arrest, prompt tracheal intubation and mechanical ventilation is life-saving.

Gneral anesthesia for ceserean section

Aspiration prophylaxis.

–Pre-induction administration of nonparticulate antacid such as 0.3 M sodium citrate, 30 mL.

–Intravenous administration of histamine receptor blocking agent 40 minutes before induction.

–Administration of metoclopramide to decrease gastric volume 30–60 minutes before induction.

Pre-oxygenation and denitrogenation with 100% oxygen over 3 minutes is preferred technique; however, if not feasible; patient can be advised to take 8 vital capacity breaths of 100% oxygen in one minute.

If blood pressure is high, rapid control of blood pressure can be achieved by:

–Hydralazine (5 mg IV aliquots up to a maximum of 20 mg)

–Labetalol (5–10 mg IV every 10 min)

In resistant cases, infusion of sodium nitroprusside and glyceryl trinitrate may be needed. But in these cases continuous arterial pressures monitoring should to be instituted.

Consider arterial line placement before induction in patients with severe pre-eclampsia.

Anticipate difficult airway, keep small size tubes, gum elastic boogie, LMA and difficult airway set ready. Plan for attenuation of response to laryngoscopy.

Crash induction using thiopentone sodium or propofol (if blood pressure is high) in titrated doses and succinylcholine after checking ability to ventilate.

Magnesium sulfate potentiates the effects of both depolarizing and non-depolarizing muscle relaxants. One may consider use of non-depolarizing muscle relaxant, atracurium, for maintenance of neuromuscular block once the patient has demonstrated recovery from succinylcholine or small intermittent doses of succinylcholine can be used. It is preferable to use a peripheral nerve stimulator in the intraoperative period.

Use two-thirds of the MAC of inhalation agent to ensure adequate depth of anesthesia (MAC requirement decreases in pregnancy).

Watch for hemodynamic changes during delivery and removal of placenta. Fluid boluses should be given if hypotension develops.

Pre-eclampsia is a relative contraindication to use of ergot alkaloids because of the risk of hypertensive crisis.

The concerns in postpartum period

Provide adequate analgesia using titrated doses of opioids like tramadol. NSAIDs should be avoided in view of renal dysfunction and low platelets. Paracetamol should be used carefully in patients with deranged liver enzymes. Monitor urine output. MgSO4 should be continued for at least 24 hours postpartum. Maintain hemodynamic control with antihypertensives.

MANAGEMENT OF THE HEAD INJURED PATIENT

2015-01-05T12:29:00.000+03:00

Head injury can be subdivided into primary and secondary head injury. Primary injury refers to the initial injury, whilst secondary injury refers to factors which exacerbate the primary injury after the injury has occurred. The principles of management of severe head injury are aimed at preventing, or at least minimising, secondary injury.

NEUROPHYSIOLOGY RELEVANT TO SEVERE HEAD INJURY

A key factor in minimising secondary injury is avoiding cerebral ischaemia, by both maintaining

adequate cerebral blood flow (CBF) and avoidance of conditions that increase oxygen consumption by cerebral tissues.

Hypoxia, hypotension, raised intracranial pressure (ICP) and anaemia all lead to a reduction in the delivery of oxygenated blood to cerebral tissues. Hyperthermia and epilepsy both increase cerebral metabolic rate, and therefore cerebral oxygen consumption. In addition, both hypoglycaemia and hyperglycaemia are associated with a worse outcome.2

INITIAL ASSESSMENT AND MANAGEMENT OF THE HEAD INJURED PATIENT

Assessment

A systematic approach to evaluation and initial management, such as that proposed by Advanced Trauma Life Support, should be adopted for these patients.

Airway patency should be assessed and the cervical spine immobilised. The airway should be secured, by tracheal intubation, in patients who do not have a patent airway or who are significantly obtunded (GCS ≤ 8). The chest should be examined and any life-threatening injuries (e.g. tension pneumothorax, open pneumothorax, massive haemothorax, flail chest, cardiac tamponade) promptly treated.3

The circulatory state should be assessed using clinical parameters such as blood pressure and heart rate.

Any sites of external haemorrhage should be directly compressed. Patients with suspected or confirmed on-going haemorrhage will require operative intervention.

An assessment of the patient’s Glasgow Coma Score (GCS) and pupillary reflexes should be made. In addition, the presence of any lateralising neurological signs, and, in the case of spinal cord injury, a documentation of the level of altered sensation, should also be noted.

The patient should be completely exposed to assess for other injuries, whilst taking care to prevent hypothermia. All aspects of the primary survey should be completed and identified life-threatening conditions treated, before commencing the secondary survey.

Specific Neurological Assessment and Investigation

The Glasgow Coma Score is used to formally assess the conscious level of the patient. This score,

illustrated in Table 1 below, is composed of 3 components: eye-opening, verbal and motor response.

The best response in each component is used to calculate the final score, which ranges from 3, at worst, to 15, at best.

Table 1: Glasgow Coma Score3

Pupillary size and response to light should be assessed and recorded. Ipsilateral pupillary dilatation, unreactive to light, may indicate life-threatening intracranial pressure. In this situation, pupillary dilatation results from compression of the oculomotor nerve against the tentorium. Alternative causes include ocular trauma and the administration of certain drugs.4

Early symptoms and signs associated with raised intracranial pressure include headache, nausea and vomiting, seizures, papilloedema and focal neurology. Late signs of raised intracranial hypertension include a decrease in conscious level, hypertension and bradycardia (Cushing’s reflex) and an abnormal respiratory pattern. Pupillary dilatation, decorticate posturing (leg extension, arm flexion) and decerebrate posturing (leg and arm hyperextension) occur prior to coning and brain death.

Eye opening

Spontaneous 4

To voice 3

To pain 2

No response 1

Motor response

Obeys commands 6

Localises a painful stimulus 5

Flexion away from a painful stimulus 4

Abnormal flexion 3

Extension 2

No response 1

Verbal response

Orientated 5

Confused conversation 4

Inappropriate words 3

Incomprehensible sounds 2

No response 1

Box 1: Guidelines for urgent CT scanning in head injury

• GCS < 13 on initial assessment

• GCS < 15 on assessment 2 hours post-injury

• Definite or suspected open or depressed skull fracture

• Signs of basal skull fracture (e.g. Battle’s sign)

• Post-traumatic seizure

• Focal neurological deficit

• >1 episode of vomiting

• Any history of amnesia or loss of consciousness post-injury in a patient

who is coagulopathic (clotting disorder, warfarin treatment)

Indications for involvement of the neurosurgical team following head injury are listed in Box 2 below.

The exact definition of “surgically significant abnormalities” is determined by the local neurosurgical unit.

Box 2: Guidelines for neurosurgical referral in head injury

Presence of new, surgically significant abnormalities on imaging

• GCS ≤ 8 after initial resuscitation

• Unexplained confusion lasting > 4 hours

• Deterioration in GCS after admission

• Progressive focal neurological signs

• Seizure without full recovery

• Definite or suspected penetrating injury

• CSF leak

Initial Management

Airway

Indications for intubation following head injury are listed in Box 3 below.

If the cervical spine has not been cleared manual in-line stabilisation is required for intubation.

The dose and type of induction agent(s) chosen should be selected with the aims of rapidly securing the airway with minimal haemodynamic disturbance and minimal rise in ICP. With the exception of ketamine, all intravenous induction agents cause a reduction in cerebral blood flow, cerebral metabolism and intracranial pressure. In circumstances where ketamine is the only available induction agent it should be used with caution as it causes a rise in intracranial pressure. The use of intra-arterial monitoring, sited pre-induction, allows more rapid detection and treatment of hypotension.

In the uncomplicated airway a modified rapid sequence induction using a pre-determined dose of thiopentone or propofol together with an opioid (alfentanil, fentanyl) and suxamethonium can be used.

The use of an opioid obtunds the pressor response to laryngoscopy and the associated, potentially life- threatening rise in intracranial pressure. A vasopressor, such as metaraminol, should be readily available to counter any hypotension.

Although suxamethonium may itself cause a rise in intracranial pressure, this is rarely clinically

significant as is offset by the reduction in intracranial pressure caused by the induction agent. The benefits of suxamethonium in facilitating adequate intubating conditions, as well as its short duration of action are often deemed to outweigh this risk in practice.

With the availability of sugammadex, rocuronium can be used as an alternative to suxamethonium.

Following intubation and confirmation of endotracheal placement, the tube should be well secured in a fashion that ensures venous return is not obstructed. This is most easily achieved using tape rather than a cloth tie.

Box 3: Indications for Intubation Post-Head Injury1, 1

Airway

o Loss of airway reflexes

o Significant bleeding into the airway

• Breathing

o Hypoxia - PaO2 < 13kPa (98mmHg) on oxygen

o Hypercarbia - PaCO2 > 6kPa (45mmHg)

o Spontaneous hyperventilation causing PaCO2 < 4kPa

(30mmHg)

o Irregular respirations

• Disability

o GCS ≤ 8

o Seizures

• Other

o Before transfer to neurosurgical unit AND

§ Bilateral fractured mandible

§ Deteriorating conscious level (a decrease of 1 or more

points in the motor component of the GCS)

Breathing

Both hypoxia and hypo- and hypercapnia should be avoided in patients with head injuries as these worsen outcome. Hypoxia, as defined as a SaO2 < 90% or PaO2 < 8kPa (60mmHg), increases morbidity and mortality from severe traumatic brain injury. A target PaO2 > 13kPa (98mmHg) should be aimed for. In the ventilated patient this may require use of PEEP. Whilst this will increase ICP to a degree, hypoxia is more likely to have a detrimental effect on patient outcome.

Hypercapnia, through increasing cerebral blood flow, causes a rise in ICP. Conversely, hypocapnia, although lowering ICP, also lowers cerebral perfusion and may worsen ischaemia. To achieve adequate cerebral perfusion, without significantly increasing ICP, a PaCO2 of 4.5 – 5.0kPa (34-38mmHg) is targeted. In the patient with clinical or radiological evidence of intracranial hypertension modest hyperventilation can be instituted, but maintaining PaCO2 above 4kPa (30mmHg).

In the ventilated patient, arterial blood gas analysis should be used calibrate end-tidal CO2 to PaCO2.

Where appropriate changes in ventilatory settings should be instituted to ensure the above target is achieved. Continuous capnography should be used in all ventilated patients.

Circulation

Hypotension increases morbidity and mortality in severe traumatic brain injury. A cerebral perfusion pressure of 50 – 70 mmHg should be targeted. In cases where the ICP is not measured but suspected to be raised, maintenance of a mean arterial pressure of over 80mmHg should ensure an adequate cerebral perfusion pressure in all but the most severe cases of raised intracranial pressure. Once normovolaemia has been achieved a vasopressor, such as metaraminol or noradrenaline, may be required to maintain mean arterial pressure at this level and offset the hypotensive effect of any anaesthetic agents used.

Box 4: Summary of Therapeutic Targets in Managing Severe Head Injury

• PaO2 > 13kPa (98mmHg)

• PaCO2 of 4.5 – 5.0kPa (34- 38mmHg)

o A lower PaCO2 , ≥ 4kPa (30mmHg), should be targeted with clinical or

radiological signs of intracranial hypertension

• MAP ≥ 80 mmHg (in the absence of ICP monitoring)

• Glucose 4 – 8 mmol/l

• Temperature < 37°C

• If ICP monitoring in situ

o CPP 50 – 70mmHg

o ICP < 20mmHg

anesthesia fun

2015-01-05T11:50:00.002+03:00

http://www.cartoonstock.com/directory/a/anaesthetist.asp