Sub Arachnoid Haemorrhage, management in Emergency and Neuro Intensive care

Department of Emergency and Neurosurgery, Kauvery Hospital, Trichy-Cantonment, India

Background

Subarachnoid Hemorrhage (SAH) is bleeding into subarachnoid space, often due to a ruptured aneurysm.

Aneurysm SAH is most often a devastating event. Twenty percent of strokes are hemorrhagic, including SAH and Intra Cranial Hemorrhage (ICH), each accounting for 10%. Spontaneous SAH is caused by ruptured saccular aneurysm; other causes of SAH include trauma, Arterio-Venous Malformation (AVM), fistula, vasculitis, intraarterial dissection, amyloid angiopathy, bleeding diathesis and illicit drugs (cocaine and amphetamine).

Medical management of SAH focuses on reducing the risk of secondary complications – specifically rebleed, seizures, hydrocephalus, vasospasm, and delayed cerebral ischemia. Initial measures to reduce the risk of neurological and systemic complications should be started early in the emergency department at the time of presentation and further managed in the neuro intensive care unit.

Definitive management includes surgical clipping and endovascular coiling.

In this article, we discuss the medical management of SAH patients in our neuro intensive care.

Case Presentation

A 16-year-old male presented to the ER at Kauvery Specialty Hospital with complaints of headache and vomiting for 15 days. Patient had a history of cystitis and left pyelonephritis, and was treated with ceftriaxone in an outside hospital. However, he had persistent headaches and vomiting, and was hence referred to Kauvery Hospital.

On arrival at ER patient’s GCS was E4 V5 M6, HR: 75, BP: 130/80 mmHg, SpO2: 99% on RA. CT brain and angiography imaging showed saccular aneurysm arising from Anterior Communicating Artery (ACOM), absent AI segment of left Anterior Communicating Artery (ACA), and acute SAH in the suprasellar cistern. Echo showed normal chambers, no RWMA, and good LV function. Initial blood labs normal, urine c/s: sterile.

In ER patient was managed with IV fluids of 100ml / hr, analgesics for headache, and nimodipine. His WFNS score was 1. He was then shifted to ICU and planned for surgery. On receiving at ICU, patient was electively intubated, right subclavian central venous line and right radial arterial line were secured. He underwent right pterional craniotomy with clipping (on table ruptured aneurysm was noted).

Post operatively patient was received in neuro ICU and managed with IV fluids of 125 mL/hr of crystalloids, antibiotics, analgesics, calcium channel blockers (nimodipine) and ionotrops to maintain high normal BP. Post operatively patient had persistent fever; broad spectrum antibiotics were instituted. Blood and urine cultures were sterile. Patient’s condition clinically improved and was liberated from mechanical ventilation. Inotropes were tapered and stopped and antibiotics deescalated. Patient became clinically stable and was discharged home on 10th postop day.

Fig. 1. Preoperative CT Brain.

Fig. 2. SAH noted in anterior IHF and suprasellar cistern.

Fig. 3. CT Angio show ACOM Aneurysm.

Fig. 4. Postoperative CT Brain

Guidelines for management of SAH

Critical care management

Stabilization: Initial care of patients with SAH is directed at reversing or stabilizing life-threatening conditions, particularly for comatose patients. Important steps include ensuring a secure airway, normalizing cardiovascular function, treating seizures, discontinuation of antithrombotics, and reversal of anticoagulation if present.

Indications for endotracheal intubation: include a Glasgow Coma Scale (GCS) score <=8, elevated intracranial pressure (ICP), poor oxygenation or hypoventilation, hemodynamic instability, and requirement for heavy sedation or paralysis.

Acute care: The most important goal of SAH management is the prevention of rebleeding by early repair of the unsecured aneurysm with surgical clipping or endovascular coiling.

A number of grading systems are available to classify and prognosticate aneurysmal bleed.

Grading severity of SAH: The degree of neurologic impairment and the extent of subarachnoid bleeding at the time of admission are the most important predictors of neurologic complications and outcome.

The grading system proposed by Hunt and Hess and that of the World Federation of Neurological Surgeons (WFNS) are among the most widely used.

Post-operative care measures to reduce the risk of neurologic and systemic complications, particularly vasospasm and delayed cerebral ischemia, involve blood pressure management, maintenance of euvolemia, treatment with nimodipine, and continuous monitoring for hemodynamic and neurologic complications.

Additional acute measures include bedrest, analgesia, venous thromboembolism prophylaxis, and discontinuation of antithrombotics (plus reversal of anticoagulation when present). Hypoxemia, hyperglycemia, fever, and cardiovascular instability are common complications associated with poor outcome and should be prevented and promptly treated.

Euvolemia is the goal of intravenous fluid administration, usually with normal saline, monitored meticulously. Hypovolemia is the risk factor for vasospasm and ischemic complication. Fluid administration should also target normal electrolyte balance. Hyponatremia, in particular, is common and thus serum sodium is checked every day.

Optimal methods to monitor volume status includes strict intake output chart, CVP, echocardiography to see IVC variability

Triple H therapy (hypervolemia, hypertension, haemodilution) has been considered for many decades to increase cerebral blood flow in aneurysm SAH to prevent and treat cerebral vasospasm. At current time Triple H and its components not proved to increase cerebral blood flow in SAH patient.

Blood pressure management: The goal is to maintain systolic blood pressure (SBP) <160 mmHg or mean arterial pressure (MAP) <110 mmHg in unruptured and secured aneurysm. It is reasonable to use premorbid baseline blood pressure to refine these targets. Hypotension should be avoided.

Intravenous labetalol, nicardipine, clevidipine, or enalapril are preferred to control Blood pressure if MAP is more than 110 mmHg. Nitroprusside or nitroglycerin should be avoided as the increase cerebral blood flow and thereby ICP.

The patients given antihypertensive therapy had a lower incidence of rebleeding that was offset by a higher incidence of infarction.

Induced hypertension produces modest increase in cerebral blood flow and is recommended in delayed cerebral ischemia, provided the aneurysm has been secured. The goal is to increase the MAP by 20 % of the previous blood pressure.

Preferred vasopressors include norepinephrine, phenylephrine and dopamine.

Haemodilution done by adequate hydration with crystalloids.

Nimodipine: Nimodipine has been demonstrated to improve outcomes. Crystalloids are standard of care in these patients and the mechanism includes neuroprotection via dilation of small arteries and not visible on angiogram and reduction of calcium ddependentexcitotoxicity, diminished platelet aggregation, inhibition of ischemia triggered by red blood cells product and some combination of these actions. Nimodipine 60 mg every four hours is administered to all patients with aneurysmal SAH starting within 48 hours of symptom onset, or sooner once the patient is stabilized. Nimodipine must be given orally or by nasogastric tube. Treatment is continued for 21 days.

Intraarterial BP monitoring is essential to avoid hypotension and decrease cerebral perfusion pressure.

Seizure prophylaxis is initiated for patients with poor neurological grade and secured aneurysm with ICH. Phenytoin is been associated with worst neurological and cognitive outcome after SAH, thus should be avoided. In the absence of seizures antiepileptics should be discontinued once aneurysm is secured.

In the absence of acute seizures, antiseizure medication therapy should be discontinued in most patients after the aneurysm is secured.

Pain control: For pain control of headache, neck pain, and other sources of pain paracetamol along with short-acting opiates are used avoiding aspirin before aneurysm is secured.

Early complications

Medical and neurological complication are common after SAH and contributes to the overall morbidity and mortality. Neurological worsening occurs in approximately 35% of patients within first 24 h of SAH and is associated with high mortality as high as 70%. Early complication includes Rebleeding in the first 24 h substantial risk for early rebleed in 4-14%. Re-rupture is associated with high mortality.

Predictor of rebleeding

Most rebleeding is into subarachnoid space, intraparenchymal, Interventricular or subdural compartment. It is clinically recognised by acute deterioration of neurological status and diagnosed by CT brain.

Vasospasm and delayed cerebral ischemia (DCI)

Delayed cerebral ischemia occurs in approximately 30% of patients with aneurysmal SAH and between 4-14 days after symptom onset. It is characterised by new onset focal neurological impairment or decrease by at least 2 of GCS that last for an hour and not attributable to any other systemic or metabolic cause. Prevention of DCI includes maintenance of euvolemia and early initiation of nimodipine. Haemodynamic augmentation is to increase MAP and CPP is the first line therapy for new onset DCI.

Vasopressors such as phenylephrine, Dopamine are used. Inotropes such as dobutamine, noradrenaline are helpful in patient who does not respond to vasopressors and who have left ventricular dysfunction.

Earlier version of this therapy is triple H therapy where in studies revealed Hypovolemia was not beneficial and may be harmful in LVD patients

Intra-arterial administration of vasodilators such as papaverine, milrinone, nicardipine are used.

Elevated ICP: It is due to number of factors including hemorrhagic bleed, acute hydrocephalus, reactive hyperemia and distal cerebral arteriolar vasodilatation and prevention of even good HESS AND HUNT graded 1 to 3 in these patients.

Hydrocephalus: Affect 20-30 % of patient with SAH, occur in few minutes to hours after SAH and can also be a later complication. There is a progressive deterioration of active level of consciousness with or without ocular sign along with ventricular dilatation in head CT scan. Acute hydrocephalus is associated with increased morbidity and mortality secondary to rebleeding and general infection.

Hyponatremia: Develops in 30 % of SAH Patients due to hypothalamic injury. It is mostly due to SIADH and rarely due to salt wasting syndrome. Diuretics and fluid restriction is given and monitored continuously.

Monitoring: constant hemodynami, cardiac and neurological monitoring are done in intensive care setting

Arterial blood pressure is monitored to maintain adequate MAP and CPP

CVP for monitoring volume status along with measurements of inferior vena cava diameter variability in ECHO.
ICP monitoring in patient with hydrocephalus EVD is done for CSF drainage and monitoring ICP.
TCD sonography done to detect and monitor vasospasm in SAH.
Brain and vascular imaging – DSA and CTA are done to detect vasospasm and delayed ischemia of brain.
CBC is done for anaemia and infection.
Renal parameter especially sodium is constantly monitored and corrected accordingly.
Cardiac monitoring: ECHO is done preoperatively and also done to assess the worsening of previous LVD and stress cardiomyopathy.

Conclusion

SAH is a devastating clinical event with substantial mortality and high morbidity. Mortality within the first 30 days after SAH approaches 30 % and attributed largely to the effects of initial and recurrent bleeding, thus early stabilisation and post- operative management of intensive care is of utmost importance despite the definitive procedure of surgical clipping and coiling.

Sub Arachnoid Haemorrhage, management in Emergency and Neuro Intensive care