Intracranial Bleeds

Sub-Arachnoid Hemorrhage 
Aneurysms occur most frequently at the bifurcations of the basal cerebral arteries, implying a hemodynamic effect to the vessel wall. Almost all of the SAH is due to ruptured berry aneurysms. Other important causes include trauma, cocaine abuse, AV malformations and vasculitis. HTN, smoking and HLP are strongly associated with development of aneurysms. 
Cause of acute mortality in SAH include direct neural destruction from the force of the extravasated blood, cerebral ischemia secondary to acute elevations in intracranial pressure (ICP), and sudden death attributed to sympathetically mediated ventricular arrhythmias. Cerebral ischemia may occur at the time of aneurysmal rupture as ICP levels approach mean arterial pressure (MAP). 
Among those patients who reach a tertiary medical center safely, 25% die over the succeeding 2 weeks. Mortality for this group occurs primarily from the residual initial deficit, aneurysmal rebleeding, and the development of ischemic deficits secondary to cerebral vasospasm. The immediate concern for the patient who survives the initial SAH is rebleeding. 
Rupture of an aneurysm releases blood directly into the cerebrospinal fluid (CSF) under arterial pressure. The blood spreads quickly within the CSF, rapidly increasing intracranial pressure. The blood often spreads into the intraventricular space, but can also spread into the brain parenchyma or rarely, the subdural space, depending on the location of the aneurysm. The bleeding usually lasts only a few seconds, but rebleeding is common and occurs most often within the first day. 
Hydrocephalus after SAH is thought to be caused by obstruction of cerebrospinal fluid (CSF) flow by blood products or adhesions, or by a reduction of CSF absorption at the arachnoid granulations.  
Perimesencephalic SAH is never associated with intra-ventricular extension. 
The typical presentation of a patient who has SAH is the paroxysmal onset of a severe diffuse headache accompanied by vomiting and occasionally a variable period of loss of consciousness. The headache often is described as ‘‘the worst headache of my life.’’ The patient may develop meningismus, retinal hemorrhages, or focal neurologic signs.  
CT head: The cornerstone of the diagnosis is a noncontrasted head CT.  CT Scan non-contrast showing blood in basal cisterns (SAH) – so called “Star-Sign. 
                                              Image result for star sign subarachnoid hemorrhage
Patients who have suspected SAH and a negative CT scan must have a follow-up lumbar puncture. Findings consistent with subarachnoid hemorrhage include an elevated opening pressure, an elevated red-cell count that does not diminish from tube 1 to tube 4, and xanthochromia.  Xanthochromia is representative of the presence of bilirubin in the CSF; it requires at least 12 hours to develop and is cleared by 2 weeks post-SAH. Avoid LP in patients with focal neurologic signs, obtundation, and possible signs of increased ICP. It may induce cerebral herniation. 
Thus, patients who present to the emergency department outside of this time period may need cerebral angiography to determine definitively if a cerebral aneurysm is present. The decision possibly to delay a lumbar puncture must be balanced with the risk of rebleeding during this time. The classic findings of SAH are an elevated opening pressure and an elevated red blood cell (RBC) count that does not diminish from CSF tube one to tube four.  
When the diagnosis is in doubt, cerebral angiography needs to be performed. Cerebral angiography remains the definitive test in the diagnosis of cerebral aneurysms and it helps identifying the vascular lesion responsible for SAH. MRA is equally effective in diagnosis.  
In approximately 20% of cases, cerebral angiography after SAH does not define an aneurysm. It is critical to repeat the angiogram in 4 to 14 days if the initial angiogram is negative.  Repeat angiography performed a few days to a week after the initial angiography reveals an aneurysm in approximately 2% of overall cases and in approximately 10% of cases of perimesencephalic blood.   If repeat angiogram does not reveal an aneurysm, MRI of brain should be performed to uncover a possible vascular malformation of the brain, brain stem, or spinal cord.
Nonaneurysmal causes of SAH include perimesencephalic hemorrhage (blood in the cisterns around the midbrain), trauma, cerebral amyloid angiopathy, cocaine abuse, dural arteriovenous fistulas, arterial dissections, pituitary apoplexy, and drug use. 
Clinical Findings: 
Hydrocephalus occurs in approximately 20% of patients who have SAH. Patients may present with, or develop within hours, a communicating hydrocephalous from the acute bleed or an obstructive hydrocephalus from intraventricular extension of the hemorrhage. Ocular signs of increased ICP (miosis, downward eye deviation) occur in many but not all patients.  
Elevation of cardiac enzymes associated with ST depression, QT prolongation, large inverted T-waves and elevated BNP are common. Massive catecholamine release may lead to formation of neurogenic pulmonary edema. Neurogenic cardiomyopathy may ensue and sometimes causes sudden cardiac death. Always get an ECHO. 
Hyponatremia is common after SAH and may reflect appropriate or inappropriate ADH release, cerebral salt wasting, or a combination of the two. 
Currently, the two main therapeutic options for securing a ruptured aneurysm are microvascular neurosurgical clipping and endovascular coiling. Patients who undergo clipping or coilng should have a followup vascular imaging. 
The initial management of SAH assumes the principles of basic life support, including ensuring adequate airway, ventilatory, and circulatory support.  Admission EKGs, chest radiographs, serum electrolytes, hematology panel, cardiac and hepatic enzymes, coagulation parameters, and cross matching of blood should be performed. 
Patients should be placed on bed rest, have adequate IV access, and have an arterial line placed for monitoring vital signs. Care should be taken to avoid oversedation, which can be misinterpreted as neurologic worsening. Stool softeners should be prescribed.  Control pain to reduce ICP.
Endotracheal intubation in a patient who has a ruptured unsecured intracranial aneurysm must be performed carefully to avoid the extremes in cerebral perfusion that can occur. Lidocaine should be given before endotracheal tube placement to depress the cough reflex. Propofol and etomidate are effective short-acting aneaesthetics that do not impair cerebral blood flow (CBF). 
Triple H therapy: Hemodilution with fluids, hypertension (but not >160) and hypervolemia seem to improve cerebral blood flow. However, this concept is controversial now. Infact, AGG/AHA recommends against hypervolemia. 
The goal is to prevent hypovolemia and to maintain cardiac output (Can use dobutamine to augment cardiac output if needed). Maintain an adequate cerebral perfusion pressure but at the same time, treat high blood pressures as the risk of rebleeding is very high. Goal blood pressure is not clearly established but a target of systolic blood pressure less than 160 is reasonable. Agents of choice are labetalol, hydralazine, esmolol and nicardipine. If vasopressors are needed to maintain adequate cerebral perfusion, norepinephrine is the 1st choice. 
Prophylactic anticonvulsants currently are recommended in the immediate posthemorrhage period, based on the concern that a posthemorrhage seizure could promote rebleeding.  
Cerebral Vasospasm: After the aneurysm is repaired, or ‘‘protected’’ from rebleeding, the focus of medical management of the patient shifts to identifying, monitoring, and preventing the neurologic complications of cerebral vasospasm.  
Cerebral vasospasm is a pathologic narrowing of the cerebral arteries occurring after SAH. It is a self-limited process that develops between days 4-12 and resolves in approximately 2-3 weeks. The best predictor of vasospasm is the amount of blood seen on the initial head CT scan. Cerebral vasospasm can be treated with Nimodipine 60mg Q4hrs for 21 days (It only treats it but not prevent it). It should be started within 72-96 hours. It may cause significant hypotension, which may worsen cerebral ischemia in patients with vasospasm. Statins also has some role in reducing vasospasm.  
Transcranial Doppler (TCD) sonography is useful for detecting and monitoring vasospasm in SAH. Follow cerebral vasospasm with daily transcranial Doppler. Other methods to detect vasospasm include digital substraction angiography (Gold standard), CTA and MRA.  Once symptomatic vasospasm is evident (with focal neurologic signs), patients are treated with hypervolemia and induced hypertension to augment cerebral perfusion. 
If hydrocephalus causes symptoms, emergent EVD to drain CSF must be attempted. In patients who are sedated and have CT-proven hydrocephalus, lumbar drainage should be considered if the third and fourth ventricles are not filled with blood. 
Antifibrinolytics like aminocaproic acid (first 24–48 hr, 5 g IV, followed by infusion at 1.5 g/hr) can reduce the risk of rebleeding but also increase the risk of thrombosis like DVT. Hence, it is acceptable to use them, if the bleed is expanding or if the surgery is delayed for any other reason. However, stop them as soon as aneurysm is repaired. 
Hyperglycemia and hyperpyrexia are associated with worse outcomes and hence, need to be treated aggressively.
DVT prophylaxis is a must, first with ICD’s and then with heparin 24 hours later once aneurysm is secured.  
Intracerebral hemorrhage 
Etiologies — Hypertensive vasculopathy is the most common etiology of spontaneous ICH. Cerebral amyloid angiopathy is the most common cause of nontraumatic lobar ICH in the elderly, while vascular malformations are the most common cause of ICH in children. Additional causes of nontraumatic ICH include: 
  • Hemorrhagic infarction (including venous sinus thrombosis). 
  • Septic embolism, mycotic aneurysm. 
  • Brain tumor. 
  • Bleeding disorders, anticoagulants, thrombolytic therapy. 
  • Central nervous system (CNS) infection (eg, herpes simplex encephalitis). 
  • Moyamoya. 
  • Vasculitis. 
  • Drugs (cocaine, amphetamines) 
Mechanisms of brain injury -There are several mechanisms of brain injury in ICH: 
  • Primary direct mechanical injury to brain parenchyma by the expanding clot 
  • Increased intracranial pressure (ICP) 
  • Herniation secondary to mass effect 
Clinical Presentation In contrast to brain embolism and subarachnoid hemorrhage, the neurologic symptoms do not begin abruptly and are not maximal at onset. Headache, vomiting, and a decreased level of consciousness develop if the hematoma becomes sufficiently large. Seizures may develop and may progress into coma. 
Mainly by CT head or MRI. Primary ICH needs to be distinguished from hemorrhagic transformation of a cerebral infarction. While there are no defined radiologic criteria for this distinction, a patchy appearance of the hyperdensity within a larger area of low attenuation is an important feature.  CTA and contrast-enhanced CT may be considered to help identify patients at risk for hematoma expansion. 
Conventional diagnostic cerebral angiography should be reserved for patients in whom secondary causes of ICH are suspected, such as aneurysms, arteriovenous malformations, cortical vein or dural sinus thrombosis, or vasculitis. 
  1. Sources of fever should be treated, and current guidelines suggest the use of antipyretic medications to lower body temperature to normothermia in febrile patients with stroke  
  2. Hyperglycemia in the first 24 hours after stroke is associated with adverse outcomes, and current guidelines suggest insulin treatment to target serum glucose level between 140 to 180 mg/dL  
  3. The treatment of intracerebral hemorrhage to achieve a target systolic blood pressure of 110 to 139 mm Hg did not result in a lower rate of death or disability than standard reduction to a target of 140 to 179 mm Hg. ( ATACH 2 Trial). In older INTERACT II study, intensive blood pressure lowering ( less than 140 vs less than 180) was associated with improved measures of disability according to modified Rankin scores. 
  4. The goal blood pressure should be to target a CPP of 60-80. Drugs of choice are labetalol, nicardipine, esmolol, enalapril , hydralazine and nitroprusside. 
  5. Intermittent pneumatic compression is the mainstay for prevention of venous thromboembolism in patients with acute ICH.  
  6. Normal saline initially should be used for maintenance and replacement fluids; hypotonic fluids are contraindicated as they may exacerbate cerebral edema and intracranial pressure. Hypervolemia should be avoided as it may worsen cerebral edema. 
  7. Dysphagia is common and is a major risk factor for developing aspiration pneumonia. Prevention of aspiration in patients with acute stroke includes NPO until swallowing function is evaluated.  
  8. Aggressive use of intravenous vitamin K, unactivated prothrombin complex concentrate (also called factor IX complex), and other factors may be necessary in patients who suffer an ICH while taking warfarin. 
  9. Protamine sulfate is recommended for urgent treatment of patients with heparin-associated ICH.  
  10. For patients on antiplatelet therapy, the limited available data suggests that platelet transfusions do not improve outcomes. 
  11. PCC complex normalizes INR faster than Vit.K or FFP. ( However, PCC complex also increases the risk of thrombosis and DIC) 
  12. Outcome mainly affected by ICH volume and Intraventricular hemorrhage  
  13. Clot removal with extra ventricular device and localised tPA 1mg every 8 hrs has decreased mortality ( Clear III study).
  14. A policy of early hematoma evacuation is not clearly beneficial compared with hematoma evacuation when patients deteriorate. 
  15. Antiplatelets can be resumed after 7-10 days , provided the bleed has been stable.
  16. The optimal timing to resume oral anticoagulation after anticoagulant-related ICH is uncertain. Avoidance of oral anticoagulation for at least 4 weeks, in patients without mechanical heart valves, might decrease the risk of ICH recurrence​. In high risk patients with metallic valve, it can be resumed in 1-2 weeks, ideally with heparin intially. 
Treatment of increased ICP: 
  1. Elevate the head of the bed to 30 degrees, once hypovolemia is excluded. 
  2. Analgesia, fever control and sedation, particularly in unstable, intubated patients. Sedation should be titrated to control pain and minimize ICP elevation, while still permitting clinical evaluation of the patient's neurologic status. Do not over sedate so as to make it difficult to differentiate between clinical deterioration vs. oversedation. Bolus doses of opiates should be used with caution as they drop MAP acutely thereby decreasing CPP. 
  3. Airway should be maintained.  Preferred induction agents for rapid sequence intubation (RSI) in the setting of ICH include propofol and etomidate.  Succinylcholine can cause hyperkalemia, cardiac arrhythmias, exacerbation of neuropathy or myopathy, malignant hyperthermia, and elevation of intracranial pressure. For this reason, in neurological patients, non-depolarizing neuromuscular blocking agents, such as cisatracurium, rocuronium, or vecuronium, are preferred.  
  4. SBP should be targeted to less than 160 or MAP around 80-90 to keep cerebral perfusion pressure around 60-80. (CPP = MAP-ICP). Keep ICP less than 20. 
  5. Normal saline initially should be used for maintenance and replacement fluids; hypotonic fluids are contraindicated and may worsen cerebral edema. Mild hypernatremia should be tolerated. 
  6. Glucocorticoids should NOT be used to lower the ICP in most patients with ICH.  
  7. Dextrose-containing solutions should be avoided as hyperglycemia may be detrimental to the injured brain 
  8. Invasive monitoring and treatment of ICP should be considered for patients with GCS <8, those with clinical evidence of transtentorial herniation, or those with significant IVH or hydrocephalus.  
  9. More aggressive therapies for reducing elevated ICP include osmotic diuretics (eg, mannitol and hypertonic saline solution), ventricular catheter drainage of cerebrospinal fluid, and neuromuscular blockade with the goal of maintaining cerebral perfusion pressure (CPP) of 60 mmHg. If ICP is elevated, a target CPP of 50 is acceptable. 
  10. Intravenous mannitol is the treatment of choice to lower increased intracranial pressure, quickly and effectively lowering ICP. It is administered as an initial bolus of 1 g/kg, followed by infusions of 0.25 to 0.5 g/kg every six hours. The goal of therapy is to achieve plasma hyperosmolality (300 to 320 mosmol/kg) while maintaining an adequate plasma volume; major side effects include hypovolemia and a hyperosmotic state  
  11. Hypertonic saline with 3% or 23% can be used to decrease ICP but sodium levels should be kept less than 150-155 
  12. Barbiturate anesthesia can be used if mannitol fails to lower ICP to an acceptable range. Barbiturate coma acts by reducing cerebral metabolism, with a resultant decrease in cerebral blood flow and thus decreased ICP. Continuous EEG should be done to produce burst suppression without over sedating the patients. 
  13. Hyperventilation to a PaCO2 of 35 to 40 mmHg causes dramatic and rapid lowering of ICP. However, the effect only lasts for minutes to a few hours. Hence, this is at best a temporising measure, especially when patients are being transported.   
  14. Neuromuscular blockade is sometimes employed to reduce ICP in patients who are not responsive to analgesia and sedation alone, as muscle activity can contribute to increased ICP by raising intrathoracic pressure, thereby reducing cerebral venous outflow.  
  15. Cerebrospinal fluid drainage by intraventricular catheter placement (ventriculostomy) is an effective means of lowering ICP
  16. Emergent surgical evacuation of bleed is needed if there is any evidence of herniation. 
  17. Decompressive craniectomy can be considered if the ICP is very high. 
  18. In general, no matter how high the BP is, it should not be reduced by more than 15-30% in first 24 hours. Esmolol, labetalol, nicardipine, fenoldopam, and enalapril are ideal choices. 
  19. Prophylactic antiseizure medications should be started because any seizures will worsen ICP and may cause brain herniation. 
  20. If everything fails to treat raised ICP, therapeutic hypothermia may be considered to decrease cerebral metabolic rate. 
  • Subdural hematoma: The most common cause if cerebral atrophy, especially in elderly and chronic alcoholics. Other cause include AV malformations, coagulopathy, meningioma and dural metastasis. Surgical evacuation is recommended if there is a clot thickness >10 mm or midline shift >5 mm or if the GCS score has decreased by ≥2 points from the time of injury to hospital admission
  • CPP = MAP – (ICP or CVP), whichever is higher. 
  • The normal physiologic response of a patient who has SAH is to release large amounts of catecholamines and vasopressin. 
  • Cushing’s triad (Bradycardia, wide pulse pressure and cheyne-stokes or irregular breathing) is a sign of raised ICP. 
  • If patient needs anticoagulation in SAH, it’s okay after 24 hours, once aneurysm is secured. In contrast, all blood thinners are contraindicated in acute intra cerebral hemorrhage. The timing of restarting anticoagulation is always controversial even though most would agree after 10 days, provided BP is well controlled and risks of not starting is very high( as in stroke and CAD). Similarly, heparin can be resumed in 10 days while Coumadin can be resumed in 3-4 weeks with strict monitoring of INR. 
  • SIADH vs. Cerebral salt wasting: Very difficult to differentiate and sometimes, both may coexist. Both cause hypotonic hyponatremia with high urinary sodium. SIADH is euvolemic with oliguria and CSW is hypovolemic with increased urine output.
  • Diagnostic workup in all patients with intracranial hemorrhage include CBC, CMP, Coagulation studies, troponins, EKG, type and cross match and tox screen. 

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