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.

MANAGEMENT OF THE HEAD INJURED PATIENT

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

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 deathFollowing head injury, the diagnostic investigation of choice is a CT scan of the head. Indications for patients requiring an urgent CT scan are listed in Box 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

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Stiff Person Syndrome and Anesthesia: Case Report

1. Jans Bouw, MD*, 
2. Karin Leendertse, MD*, 
3. Marina A. J. Tijssen, MD PhD†and 
4. Misa Dzoljic, MD PhD*

+Author Affiliations

1. *Departments of Anesthesiology and †Neurology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

1. Address correspondence and reprint requests to J. Bouw, MD, Department of Anesthesiology, Academic Medical Center, University of Amsterdam, PO Box 22700, 1100 DE Amsterdam, The Netherlands. Address e-mail toj.bouw@amc.uva.nl.

Abstract

IMPLICATIONS: This case report describes the successful perioperative management of a patient with a rare and disabling neurologic disorder, the stiff person syndrome. The patient had a delayed emergence despite apparent full reversal of neuromuscular blockade. We suggest an interaction between the GABAergic effects of baclofen and volatile anesthetics as a possible cause.

Stiff person syndrome (SPS) is a rare and disabling neurologic disorder characterized by muscle rigidity and episodic spasms that involve axial and limb musculature (1–3). The literature points toward an autoimmune disorder resulting in a malfunction of γ-aminobutyric acid (GABA)-mediated inhibitory networks in the central nervous system (4). Anesthetic implications are less well described. We report a case of prolonged hypotonicity after general anesthesia in a patient with SPS and discuss the possible anesthetic interactions.

Case Report

A 62-yr-old woman (height, 1.70 m; weight, 61 kg) was scheduled for resection of a colon carcinoma. Her medical history revealed hypothyroidism, vitamin B12 deficiency, and SPS. This syndrome started with low back pain, which rendered her unable to walk. She was experiencing stiffness, involuntary jerks, and painful cramps. Neurological examination revealed extreme hypertonia of the body and proximal legs, with intercurrent, painful spasms. Reflexes were symmetrical without Babinski signs. Laboratory findings showed positive glutamic acid decarboxylase (GAD) and negative amphiphysin antibodies. The patient was successfully treated with baclofen and diazepam. Subsequently, prednisone as immunosuppressive therapy was started. The stiffness diminished, and the patient was able to walk unaided. The neurological examination was unremarkable, except for a slight stiffness in the legs. Her medication at admission was prednisone 20 mg once a day, baclophen 12.5 mg twice a day (daily dose = 25 mg), diazepam 7.5 mg twice a day (daily dose = 15 mg), levothyroxine 25 μg once a day, and vitamin B12 injections. Her medical history included urological and gynecological surgery under general anesthesia before she experienced SPS.

No premedication was given. Anesthesia was induced with propofol (2.5 mg/kg) and sufentanil (0.25 μg/kg). After the administration of atracurium (0.6 mg/kg), the trachea was intubated, and anesthesia was continued with isoflurane (0.6–1.0 vol%) and oxygen/air for the duration of the procedure. Cefuroxime 1500 mg, clindamycin 600 mg, and dexamethasone 10 mg were administered IV. In the following 2 h, additional atracurium (35 mg), sufentanil (10 μg), and morphine (8 mg) were administered. At the end of the procedure, which was uneventful, neuromuscular monitoring showed four strong twitches. Although the patient was responsive, she could not open her eyes, grasp with either hand, or generate tidal volumes beyond 200 mL. Neostigmine 2 mg (0.03 mg/kg) and glycopyrrolate 0.2 mg did not alter the clinical signs of muscle weakness.

The patient was sedated with propofol 5 mg · kg⁻¹ · h⁻¹ and further mechanically ventilated in the recovery room. After 1 h, the sedation was stopped and mechanical ventilation was terminated. At that time, baclofen 12.5 mg was administered into the gastric tube. Two hours later she was in a good clinical condition, and her trachea was extubated.

Discussion

SPS was recognized as a distinct entity in 1956 by Moersch and Woltman (5). An autoimmune pathogenesis is suspected because of the presence of antibodies against GAD, the rate-limiting enzyme for synthesis of the inhibitory neurotransmitter GABA, and the association of the disease with other autoimmune conditions such as diabetes and thyroiditis (6,7). Loss of inhibition from higher centers causes hyperactivity of the γ-motor neuron system and subsequent progressive muscle rigidity. Patients with SPS have high immunoglobulin G/anti-GAD-65 antibodies, which are synthesized intrathecally and seem to impair the in situ synthesis of GABA (8,9). Two types of drugs have been applied: drugs that enhance GABA activity and immunosuppressing drugs. Diazepam, which increases the frequency of opening of the GABA_A receptor and leads to hyperpolarization, is the initial treatment of choice at daily doses up to 200 mg. Intrathecal or oral baclofen may improve the physical symptoms just like prednisone, plasmapheresis, and large-dose IV immunoglobulin (10).

In our case, several drugs could have caused muscle weakness (11). Initially atracurium could be suspected. Computer-simulated pharmacokinetic analyses suggested that plasma concentrations were far less than therapeutic levels. The same can be said for opioids, fentanyl, and morphine (Fig. 1) (12–15). In the recovery room while the patient was still ventilated, it showed a diazepam serum concentration of 0.317 mg/L (therapeutic range, 0.125–0.75 mg/L). Because IV drugs can be excluded as causing muscular weakness, perhaps volatile anesthetics were the cause. In the case report by Johnson and Miller (10), muscle weakness was observed only when baclofen was combined with inhaled desflurane or isoflurane. Delayed arousal and muscle weakness were also described, unrelated to SPS, in a patient receiving baclofen and undergoing anesthesia with isoflurane 1% (16). In addition, recent animal studies show that baclofen enhances volatile anesthetic-induced anesthesia (17). Perhaps the complicated course of recovery was most due to the interaction between isoflurane and baclofen causing muscle weakness.

View larger version:

Figure 1. Chart showing three different drugs given during the procedure. Time 0 represents the start of the procedure, which ended after 150 min. The serum concentrations of sufentanil and atracurium, although given in different units, can be seen on the left axis, and the right axis represents serum concentrations of morphine. It is noteworthy that after the initial intubation dose of atracurium, three doses (5, 10, and 20 mg) were given during the procedure.

We thus conclude that the prolonged muscle relaxation can be explained by the enhancement of general anesthetics via GABA_B action on synaptic transmission (17). This case demonstrates a potential danger in combining baclofen with volatile anesthetics in patients with SPS.

Anaesthetic management of a case of idiopathic intracranial hypertension

Bina P Butala and Veena R Shah

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Abstract

Idiopathic intracranial hypertension (IIH) is a rare headache syndrome characterized by prolonged elevation of intracranial pressure without related pathology in either the brain or the composition of cerebrospinal fluid. Herein, we provide a brief review of the clinical presentation of IIH and the anaesthetic considerations in a female posted for transcervical resection of the endometrium and right nephrectomy with the disorder. Most of patients with IIH are reported during pregnancy and came for management of labour and delivery. To our knowledge no such case has been described previously.

Keywords: Cerebrospinal fluid, idiopathic intracranial hypertension, intra cranial pressure, lumbar puncture, papilledema

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INTRODUCTION

Idiopathic intracranial hypertension (IIH) was first described in 1893. Patients with IIH have a classical picture of headache, papilledema, and a raised cerebrospinal fluid (CSF) pressure of more than 25 mmHg. It is more common in women than in men (3:1) with the highest incidence seen in obese women of reproductive age group (20-45 years). The most common presenting symptoms are manifestations of generalized intracranial hypertension, normally headache and visual obscuration. Diplopia, pulsatile tinnitus, nausea and vomiting may be present in about 50% of patients, with neck/back/shoulder pain or radicular pain less frequent.[1] The major risk of IIH is visual loss, which may be permanent despite medical therapy. It seems that the symptoms worsen during pregnancy in 50% of the patients and usually resolve postpartum.[2]

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CASE REPORT

A 45-year-old female, weighing 70 kg presented with complaints of headache, menorrhagia and pain in the abdomen was admitted to our hospital. She was posted for transcervical resection of the endometrium and patient had a past history of headache and blurring of vision 2 years ago and was diagnosed to have IIH and was on tablet acetazolamide 250 mg every 6 h. She had a history of lumbar CSF drainage twice. Patient had a history of hypertension and was on tablet atenolol once daily. On pre-operative examination, pulse was 70/min and blood pressure was under control. Other general and systemic examination was normal. All other investigations were within normal limits. Computer tomography brain was normal and magnetic resonance imaging revealed partially empty sella and no pituitary mass lesion, cerebral hemisphere and ventricles were normal. Fundus examination revealed chronic papilledema, optic nerve pallor and perimetry showed increased size of blind spot. Neurologist advised preoperative CSF pressure measurement and drainage if pressure is high. CSF manometry was performed in the lateral decubitus position and CSF pressure was more than 250 mm H2O with normal cytological and biochemical profile. 20 mL of CSF was drained with a 22 gauge Quincke's needle. After drainage the CSF pressure was 150 mm H2O. Patient was posted for surgery after 2 days.

On the day of surgery, injection glycopyrrolate (0.2 mg), injection midazolam (2 mg) and injection fentanyl (200 μg) were given intravenously as pre-medication. Anaesthesia was induced with propofol 175 mg and tracheal intubation was facilitated with vecuronium 5 mg injection plain lignocaine 2% 5 ml was given to attenuate pressor response. Anaesthesia was maintained with oxygen, nitrous oxide, propofol infusion, and vecuronium. Intra-operatively injection mannitol 1 g/kg was given. Monitoring included pulse oximetry, electrocardiogram (ECG), noninvasive blood pressure noninvasive blood pressure (NIBP), ETCO2, urine out-put and temperature. At the end of surgery neuro-muscular block was reversed with injection neostigmine 3.5 mg and glycopyrrolate 0.4 mg. She was shifted to post-operative recovery room and monitored for 48 h with pulse oximetry, ECG, NIBP, urine out-put, and temperature. She was completely asymptomatic at discharge.

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DISCUSSION

IIH was first described by Quinke in 1893 and was called “serous meningitis.” IIH is caused by dural sinus thrombosis, a reduction in corticosteroid therapy, hormonal imbalance, vitamin A toxicity, anabolic corticosteroids, long-term tetracycline, hormonal contraceptives, lithium, and pregnancy.[3] Theories of IIH pathophysiology include increased venous sinus pressure, decreased spinal fluid absorption, increased spinal fluid secretion, increased blood volume and brain oedema.[4] The various treatment modalities used in patients include corticosteroids, acetazolamide, diuretics, repeated lumbar puncture and surgery. The goals of treatment of IIH involve a reduction of intracranial pressure to control symptoms and prevent pressure on the optic nerve and optic meninges, preserving vision. Serial lumbar punctures have a success rate of 30-40% when used alone. Generally, up to 30 ml of fluid is withdrawn to lower the intracranial pressure to normal.[5] Our patient had a history of IIH since 2 years, was on tablet acetazolamide and showed response to medical therapy. Lumbar puncture was carried out twice to improve symptoms. In our patient, 20 cc of CSF was removed to keep the CSF pressure within normal limits.

From the literature, it has been found that IIH is more common in females in the age group 20-45 years.[5] Women with more than 10% over their ideal body weight are 13 times more likely to develop IIH.[5] Our patient was having a body mass index of >30 kg/m2. The mechanism proposed is that central obesity raises intra-abdominal pressure, which increases intra-pleural pressure and cardiac filling pressure, which in turn impedes venous return from the brain and leads to increased intracranial venous pressure, and increased intracranial pressure.[5]

Neuraxial anaesthesia, spinal or epidural has been used successfully for caesarean section in patients with IIH. Since lumbar puncture for CSF drainage is a therapeutic modality for IIH, there is no indication to withhold spinal anaesthesia in these patients.[5] Bedson and Plaat reported the combined spinal-epidural technique for delivery by caesarean section.[1] Although, dural puncture is contraindicated in patients with increased intracranial pressure resulting from space occupying lesions due to risk of uncal herniation. However, it has been postulated that the uniform swelling and stiffness of the brain in IIH prevents herniation.[5] Aly and Lawther reported a case of uncontrolled IIH successfully managed using an epidural catheter for analgesia in labour and delivery as well as temporary control of intracranial pressure.[1] Abouleish and Ali had given spinal anaesthesia for caesarean section in patient with IIH.[6]

In our patient, both surgeries were carried out simultaneously, so we had no option for regional anaesthesia. We have selected general anaesthesia as nephrectomy was carried out in the lateral decubitus position. If a patient with IIH requires general anaesthesia, the planned approach should minimize the risk of a rise in intracranial pressure associated with intubation, inadequate depth of anaesthesia and extubation. So, we have to take measures to avoid an increase in intracranial pressure (ICP) during the peri-operative period.

Propofol offers a number of pharmacological advantages for total intravenous anaesthesia in patients of raised ICP. It decreases cerebral blood flow and cerebral oxygen consumption and increases cerebrovascular resistance. It could offer cerebral protection.[7] The synthetic short acting opioids like fentanyl lack any significant effect on ICP.

Induction and intubation may aggravate intracranial hypertension. Liberal doses of propofol combined with narcotics to achieve adequate depth of anaesthesia, mild to moderate hyperventilation, intravenous lignocaine bolus are the measures that prevent dangerous increase in ICP. We induced the patient with (200 μg) fentanyl and propofol and avoided succinylcholine for intubation as muscle fasciculation caused by succinylcholine, increase the intra cerebral blood volume and increase the ICP. Intubation in lighter planes of anaesthesia should be avoided. Atracurium causes histamine release, slightly increases the pulse rate and central system excitement, so we have used vecuronium in our patient. Vecuronium does not alter ICP or CSF dynamics and lack of cerebral effects have made vecuronium a popular choice in patients with raised ICP. Definitive measures used for decreasing the ICP include, mild head elevation, maintain EtCO2 between 25 mmHg and 30 mmHg, I.V. mannitol, continuous infusion of thiopentone or propofol, avoid hypoxia, hypercarbia, hyperthermia and hypotension.

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CONCLUSION

In conclusion, although IIH is rare, there are special considerations for anaesthetic management in patients with this disorder. Even though, these patients have an elevated ICP, anaesthesia does not cause any detrimental effects in patients with IIH. So, we have to take measures to avoid increase in ICP during the perioperative period. Despite the presence of raised ICP in these patients, there is no specific contraindication to either spinal or epidural anaesthetic technique since uncal herniation does not occur in these patients. The main goal is to avoid further increases in ICP.