CASE PRESENTATION

A 53 years gentleman, with known rheumatoid arthritis presented to the ER with complaints of:

• Sudden onset of right upper limb weakness and right lower limb weakness after intense activity.
• A history of clenching of teeth for approximately 3 seconds followed by drowsiness.
• A history of 2 episodes of vomiting containing food particles, non-bilious and non-bloodstained.

There was no associated history of headache, visual disturbances or trauma.

• A thorough review of family and personal history had no other possible cause for this condition.
• The patient is not on any blood thinners.

On examination in the Emergency Room:

• PR-102/min,
• BP-130/90mmhg,
• SPO2-99% on room air,
• CBG-155mg/dl,
• RR-24/min
• GCS-E1V1M2

Detailed Neurological Examination:

• Drowsy and on postictal confused state.
• Bilateral pupils equally reacting to light- 2mm.
• Examination of the upper limb and lower limb:

• Cerebellar signs and Tandem Walking: Could not be assessed.

INVESTIGATIONS DONE :

After obtaining an urgent Neurologist opinion, the patient was shifted for CT Brain.

CT BRAIN showed:

• Large acute intra-parenchymal hematoma in the left parieto-occipital lobes and posterior gangliocapsular region with mass effect, midline shift and intra-ventricular extension.

Management:

• The patient was resuscitated and treated in with IV sedatives and anti-epileptics in view of status epilepticus.
• After getting consent, urgent left parieto occipital decompression craniectomy and evacuation of ICH with lax duroplasty was done. The postoperative period was uneventful.
• The patient was treated with IV fluids, IV antibiotics, analgesics and other supportive measures.
• The patient stayed in ICU for 2 days and was transferred to SICU post-extubation and subsequently transferred to the ward.
• The operative drain was removed on POD 4. The patient was clinically stable and hence was discharged after 2 weeks with prescribed diuretics, antiepileptics, laxatives, etc.
• The patient was advised to continue physiotherapy and speech therapy.

Postoperative CT Brain showed:

• Residual intra parenchymal hematoma within the left posterior subcortical region along with post-op changes and air pockets.
• Minimal mass effect effacing the temporal horn of the ipsilateral lateral ventricle and regional cortical sulci
• Minimal intra-ventricular hemorrhage
• Left anterior frontal post-op pneumocephalus.

DISCUSSION:

• Intracranial hemorrhage has been associated with sexual activity. A case of intracranial hemorrhage following sexual activity is presented to further elucidate the role of physiologic response as a trigger.
• Spontaneous ICH is nontraumatic bleeding into the brain parenchyma.
• We presented a case of post-coital ICH which suggests that physical effort during sexual intercourse could have caused the ICH in association with hypertension or aneurysmal bleed or vascular malformation.
• Our patient had no cognitive impairment, no neoplasms was not a drug abuser. So we conclude that increase physical effort could have caused increased venous congestion and the rupture of an aneurysm.

CONCLUSION:

• Hemorrhagic stroke is the second most common subtype of stroke. Some of the causes include chronic hypertension, anticoagulants therapy, arteriovenous malformation, aneurysm, cavernous angioma, neoplasm, coagulopathy, etc.
• SAH due to aneurismal rupture secondary to raised intracranial pressure is the most common cause in age groups of 20 to 60.
• Approximately 50% of the mortality occurs within the first 24 hours, which emphasizes the critical importance of rapid and effective treatment in the Emergency Department. The 30 day mortality rate is between 35 to 52%. Of the survivors, 20% can be expected to regain full functionality after 6 months.
• Haemorrhagic strokes are associated with increased mortality and morbidity rates as compared to ischemic strokes. Intraventricular hemorrhage (IVH) occurs in approximately 45% of patients with spontaneous ICH and is an independent factor associated with the poor outcome which increased the risk of death from 20% without to 51% with IVH.
• Most patients who die of ICH do so during initial acute hospitalisation and these deaths usually occur in the setting of withdrawal of support because of presumed poor prognosis.
• Intracranial hemorrhage is one of the many vasculopathies that can cause brain ischaemia.

Clinical symptomatology :

• This is a medical emergency requiring immediate treatment. ICH isn’t as common as ischemic stroke, but it is more serious. Anyone can have an ICH, but the risk increases with age.
• The most common presenting symptom was sudden onset headache, seizures, contralateral weakness with a drop in sensorium. The build-up of blood puts pressure on the brain and interferes with its oxygen supply. This can quickly cause brain and nerve damage.
• It may also present with trouble swallowing, trouble with vision in one or both eyes, loss of balance and coordination, trouble with language skills. ICH can also cause apathy, sleepiness, lethargy, loss of consciousness, confusion and delirium.

Pathophysiological Mechanisms

• These are typically a manifestation of underlying small vessel disease.
• Long standing hypertension results in hypertensive vasculopathy which is known as lipohyalinosis – degenerative changes in the walls of small and medium penetrating vessels.
• Although the causes and underlying mechanism of the deposition of amyloid-beta peptide in the walls of small leptomeningeal and cortical vessels are unknown, the results include luminal narrowing, microaneurysm formation, microhemorrhages, loss of smooth muscle cells and wall thickening.
• The hematoma after the initial vessel rupture can cause direct mechanical brain injuries. Within 3 hours of the onset of symptoms perihematomal edema, which lasts between 10 to 20 days, develops.
• In 38% of patients, the hematoma can continue to expand over the first 24 hours. Blood and plasma products can mediate the secondary injury processes which include activation of the coagulation cascade, inflammatory response and iron deposition from haemoglobin degradation.

Management of this condition:

Neuroimaging:

• Non-Contrast CT is the most commonly available tool for the diagnosis of ICH and the one that is most commonly used in the ED is non-contract CT. This may also reveal the basic characteristics of the hematoma including the extension to the vascular system, location, development of mass effect, location, presence of surrounding edema and a midline shift.
• CT Angiography is the most widely available, non-invasive technique for ruling out vascular abnormalities as secondary causes of ICH. ICH with an underlying vascular etiology on CTA, potentially changing acute management. The contrast extravasation is seen on CTA images, also known as a ‘Spot Sign’ is thought to represent ongoing bleeding and those patients appear to have a high risk of hematoma expansion, poor outcome and mortality.
• MRI: In the acute phase, gradient recalled- echo (GRE) imaging techniques T2 weighting are the best option to detect the presence of ICH and it can also detect underlying secondary causes of ICH such as tumours and the hemorrhagic transformation of ischemic stroke. Finally, for patients with poor kidney function or contrast allergies, the cerebral vasculature can be analysed without contrast using Time of Flight MR angiography.

ACUTE MANAGEMENT

• Airway: Patients with ICH are often unable to protect the airway. Rapid sequence intubation is the prefered approach in the acute setting.
• Elevated BP is very common in acute ICH and is associated with greater hematoma expansion, neurological deterioration and death. Acute lowering of systolic BP to 140mmHg is safe. The AHA recommends intravenous antihypertensives with short half-lives.
• Hemostatic therapy will provide benefits in patients with underlying coagulopathy.
• The specific supportive measures include surveillance and monitoring of ICP, cerebral perfusion pressure, mechanical ventilation, temperature management and serum glucose.
• Currently, AHA recommends that prophylactic anti-epileptics should not be used routinely in patients with ICH. The only clear indications are the presence of clinical seizures or electrographic seizures in patients with a change in mental status.

SURGICAL INTERVENTIONS

• External ventricular drain placement may benefit from ICP monitoring and also has the ability to allow therapeutic drainage of the CSF, which is useful in patients with hydrocephalus. The AHA recommends that ICP monitoring and treatment be considered in patients with GCS score </=8, those with clinical evidence of transtentorial herniation, or those with significant IVH or hydrocephalus.
• Intraventricular thrombolysis– The evacuation of an intra-ventricular clot is currently not routinely recommended, a recent study comparing the use of intra-ventricular rtPA showed that the use of rtPA was not only feasible and safe but also showed a significantly greater rate of blood clot resolution.
• Hematoma evacuation is to decrease the mass effect related to the presence of blood as well as to minimise secondary injury. The only clear recommendation for immediate surgical intervention is in patients with neurological deterioration, brainstem compression, and/or hydrocepahalus from ventricular obstruction.
• Minimally invasive surgery may decrease the risk of surgical complications. These techniques are showing promising results, particularly in deep haemorrhages where conventional surgery showed no benefit in the past.
• Prevention of complications of immobility through positioning and mobilization within physiological tolerance plays a major role in management.

Overall Prognosis:

• First, the ICH score predicts the 30day mortality using features such as age (>70 years), ICH volume (>30ml), GCS <8 and the presence of IVH, with a higher score associated with worse outcomes.
• Spontaneous ICH accounts for approximately 15% of all strokes and is a leading cause of disability, with a one month mortality rate of 40%
• ICH survivors are at high risk of epileptic seizures, depression and cognitive impairment which may influence their functional outcome.
• Long term follow-up after ICH is needed to determine predictors of outcome.
• The AHA recommends aggressive full care early after ICH onset with the postponement of DNR orders until at least the second full day of hospitalization.

References:

• Intracranial hemorrhage J. Alredo Caceres, MD and Joshua N. Golstein, MD, PhD.
• Outcome of ICH Moulin S. Cordonnier C: New Insights in ICH . Front NeurolNeurosci. Basel, Karger, 2016, vol37, pp182-192.
• Guidelines for healthcare professionals from the American Heart Association / American stroke association published 28 May 2015.
• Intracerebral hemorrhage medically reviewed by Seunggu Han, M.D- Written by Ann Pietrangelo- updated on May 17, 2017
• Clinical profile and predictors of outcome in spontaneous intracerebral haemorrhage from a tertiary care in south India- Ajay Hegde, Girish Menon, Vinod Kumar, G. Lakshmi Prasad, Lakshman I. Kongwad, Rajesh nair, Raghavendra Nayak.
• Sexual activity as a trigger for intracranial hemorrhage- Paul M. Foreman, Christoph J. Griessenauer, Ajith J. Thomas Acta Neurochirurgica 158, 189- 195 (2016).

Dr Sivaranjini
2^nd Year MRCEM Resident,
Dept of Emergency Medicine, Kauvery Hospital, Chennai

Dr Aslesha Sheth
Consultant & Clinical Lead,
Dept Of Emergency Medicine, Kauvery Hospital, Chennai