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CASE REPORT Table of Contents  
Ahead of print publication
A case of resolving pontine hemorrhage


 Department of General Medicine, Srinivas Institute of Medical Sciences and Research Centre, Mangaluru, Karnataka, India

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Date of Submission13-Mar-2022
Date of Decision28-Mar-2022
Date of Acceptance30-Mar-2022
Date of Web Publication04-Aug-2022
 

  Abstract 


Generally, Pontine hemorrhages though rare have poor prognosis with 48.1% all-cause mortality noted. A grim statistic which becomes worse if the patient presents to the hospital with depressed sensorium. Level of consciousness and hemorrhage size constitute two of the most important prognostication factors for patients with pontine hemorrhage. Here we present a case of a young lady who presented with poor sensorium and a large pontine hemorrhage who went on to return to good recovery status, modified Rankin Score 2 with conservative intervention.

Keywords: Intracranial hemorrhage, pontine hemorrhage, stroke


How to cite this URL:
Rao G, Vaibhav S, Belle J. A case of resolving pontine hemorrhage. APIK J Int Med [Epub ahead of print] [cited 2022 Sep 25]. Available from: https://www.ajim.in/preprintarticle.asp?id=353261





  Introduction Top


Pons is the largest region in the brainstem bound by the midbrain superiorly, cerebellum and the fourth ventricle posteriorly and the medulla inferiorly. It connects the cerebrum to the cerebellum. The following cranial nerves originate in the pons – Cranial nerve V: trigeminal, Cranial nerve VI: abducens, Cranial nerve VII: facial, and Cranial nerve VIII: vestibulocochlear nerve. Several nerve tracts run through the pons – descending corticospinal tract, descending corticobulbar tracts, ascending medial lemniscus tracts, and ascending spinothalamic tracts. Various pontine nuclei including those that serve as apneic and pneumotaxic centers are present in the ventral pons. Pons is also home to the reticular activating system that is involved in the sleep-wake cycle. Thus, the pons is a densely functional part of the brainstem and any hemorrhage here is likely to be catastrophic. Accordingly, statistics reflect the same with many nationwide and international studies showing high mortality and morbidity associated with pontine hemorrhage.[1],[2] A combination of early measures taken to avoid secondary brain injury, fever, and infection prophylaxis and physical rehabilitation can increase the likelihood of recovery.[3]


  Case Report Top


A 37-year-old female with no known comorbidities presented to the casualty of our hospital with a history of sudden onset of unresponsiveness. A history from the bystanders revealed that the patient was in her usual state of health when she woke up in the morning at about 4:30 AM when she attended to some domestic chores and went back to sleep. She woke up at 6:30 AM and she alerted her bystanders that she could not get out of bed by gesturing. The patient could not move her right upper and lower limbs at all, having zero power. Her left upper and lower limb strength had also decreased and she was not able to lift her left upper and lower limb against gravity. The patient was taken to a nearby hospital where she was suspected to have a brainstem stroke and she was referred to the district hospital. Her sensorium progressively deteriorated. At the district hospital, her Glasgow coma scale (GCS) was recorded as 10/15 and she was referred to our hospital for further evaluation and management.

On presentation, she was having GCS of 10/15, E3V2M5. Pupils were bilaterally 2 mm, sluggishly reactive to light. She was hemodynamically otherwise stable with vital signs within physiological limits. There was quadriparesis, right upper and lower limbs comparatively more affected than the left. Her plantar reflexes were bilaterally extensor (Babinski sign positive bilaterally). Other systems (cardiovascular, respiratory, and abdominal) examination did not reveal any abnormalities.

A computed tomography (CT) scan done revealed large Brainstem hemorrhage of size 22 mm × 18 mm × 16 mm ~7 ml volume with intraventricular extension. She was admitted to the medical intensive care unit for further management. Neurosurgery opinion was taken; conservative medical management with close neurological observation was advised. She was started on anti-edema measures, broad spectrum antibiotic coverage, antiepileptics, and Ryles tube feeding. By 24 h of admission (February 20, 2021), her sensorium had further deteriorated to E1V1M4. There was complete right hemiplegia. Medical management and supportive care were continued. Hypokalemia was corrected appropriately. Investigations were done to evaluate the cause of intracranial hemorrhage in a young woman. Two-dimensional echocardiogram showed no abnormalities. Her liver function parameters, renal function parameters, bleeding time, clotting time, prothrombin time, and activated partial thromboplastin time were all found to be within normal limits. Further history elicited from her family members revealed a history of taking tablet Amitriptyline OD for an unknown psychiatric disorder. A repeat magnetic resonance imaging (MRI) brain was planned to look for vascular structural abnormalities. After 72 h in the intensive care unit, her sensorium gradually started improving. Her GCS on Day 3 (February 22, 2021) was E4V3M6. Pupils were bilaterally 3 mm, reactive to light. Quadriparesis persisted (right side > left side). Central nervous system examination on Day 4 revealed left lower motor neuron facial palsy with left abducens nerve palsy. Physiotherapy was given for limb mobilization and rehabilitation. Patients' sensorium improved and she began following orders. Her limb power gradually improved, on day 14 of admission, her right upper limb power was 3/5 and lower limb power was 4/5. Her cranial nerve deficits persisted. MRI [Figure 1] and magnetic resonance (MR) angiogram brain was done on day 14 of admission showed late subacute hemorrhage with hemosiderin rim. MR angiogram did not reveal any significant structural abnormalities. A digital subtraction angiography was planned; however, it was deferred due to financial constraints of the patient. The patient was discharged with advice on continued physiotherapy at home.
Figure 1: T2 MRI at the level of pons showing Pontine Hemorrhage (19x 18x 16mm)

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The patient was followed up and when she came for a return visit 6 months later, her neurological deficits had improved markedly with modified Rankin Score 2. She was able to speak a few words, able to comprehend speech and follow simple commands. Her power in the limbs had also improved and she was able to stand with support.


  Discussion Top


Intracerebral hemorrhage is the second-most common cause of stroke after ischemic stroke. Intracerebral hemorrhage can cause primary mechanical injury to the brain by hematoma expansion and perilesional edema. It can cause secondary brain injury from the breakdown of the blood brain barrier. The common etiological factors for hemorrhagic stroke in descending order of frequency are hypertension, amyloid angiopathy, and ruptured vascular malformations. Pons are an uncommon however typical site for hypertensive intracranial hemorrhages. Pontine hemorrhage accounts for 5%–10% of all intracranial hemorrhages.[4],[5] Primary pontine hemorrhages were classified into four types based on CT axial brain features by Chung CS, park CH:[6] (1) basal-tegmental, (2) bilateral tegmental, (3) massive, and (4) small unilateral tegmental. Our patient had bilateral tegmental type which was associated with a 26.1% mortality rate.


  Conclusion Top


Pontine hemorrhages are generally associated with poor prognosis owing to the dense nature of nerve bundle arrangement. However, in the case described above, the patient was able to achieve close to full functional status with conservative intervention aimed at preventing secondary brain injury. Most of the management was supportive. Aggressive physical rehabilitation was also given. Thus, this case is an example that poor prognosis associated with pontine hemorrhage need not be a self-fulfilling prophesy.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his/her consent for his/her images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal the identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Behrouz R. Prognostic factors in pontine haemorrhage: A systematic review. Eur Stroke J 2018;3:101-9.  Back to cited text no. 1
    
2.
Parry-Jones AR, Abid KA, Di Napoli M, Smith CJ, Vail A, Patel HC, et al. Accuracy and clinical usefulness of intracerebral hemorrhage grading scores: A direct comparison in a UK population. Stroke 2013;44:1840-5.  Back to cited text no. 2
    
3.
Matsukawa H, Shinoda M, Fujii M, Takahashi O, Murakata A. Risk factors for mortality in patients with non-traumatic pontine hemorrhage. Acta Neurol Scand 2015;131:240-5.  Back to cited text no. 3
    
4.
Wessels T, Möller-Hartmann W, Noth J, Klötzsch C. CT findings and clinical features as markers for patient outcome in primary pontine hemorrhage. AJNR Am J Neuroradiol 2004;25:257-60.  Back to cited text no. 4
    
5.
Jang JH, Song YG, Kim YZ. Predictors of 30-day mortality and 90-day functional recovery after primary pontine hemorrhage. J Korean Med Sci 2011;26:100-7.  Back to cited text no. 5
    
6.
Chung CS, Park CH. Primary pontine hemorrhage: A new CT classification. Neurology 1992;42:830-4.  Back to cited text no. 6
    

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Correspondence Address:
Gurukanth Rao,
Department of General Medicine, Srinivas Institute of Medical Sciences and Research Centre, Mangaluru, Karnataka
India
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ajim.ajim_34_22



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    -  Vaibhav S
    -  Belle J


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