LETTERS TO EDITOR
|Year : 2019 | Volume
| Issue : 4 | Page : 1159--1160
Intracranial Bleed Presenting as an Acute Cardiac Failure; Brain Heart Interaction at Its Apogee!
Ajay Prasad Hrishi P1, Karen Ruby Lionel2,
1 Division of Neuroanesthesia, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, Kerala, India
2 Department of Anesthesiology, Christian Medical College, Vellore, Tamil Nadu, India
Dr. Karen Ruby Lionel
Department of Anesthesiology, Neuroanesthesia Unit III, Christian Medical College, Vellore, Tamil Nadu
|How to cite this article:|
Hrishi P AP, Lionel KR. Intracranial Bleed Presenting as an Acute Cardiac Failure; Brain Heart Interaction at Its Apogee!.Neurol India 2019;67:1159-1160
|How to cite this URL:|
Hrishi P AP, Lionel KR. Intracranial Bleed Presenting as an Acute Cardiac Failure; Brain Heart Interaction at Its Apogee!. Neurol India [serial online] 2019 [cited 2020 Jun 2 ];67:1159-1160
Available from: http://www.neurologyindia.com/text.asp?2019/67/4/1159/266254
We report a case of intracranial arteriovenous malformation (AVM) bleed which presented as an acute cardiac failure with delayed neurological symptoms in secondary to neurogenic stunned myocardium (NSM). An AVM bleed presenting as cardiac event secondary to NSM has never been reported as evidenced by our search of the literature.
A 25-year-old male who presented with acute onset of chest discomfort and respiratory distress for 2 hours. There was no history of any cardiorespiratory illness in the past, trauma, no history of neurological disease, loss of consciousness or vomiting. Admission vitals were a heart rate of 94 beats per minutes, blood pressure of 184/98 mmHg and a respiratory rate of 38 breaths per minute. Auscultation of the chest revealed bilateral coarse crepitations in all lung fields. The pulse oximetry revealed a saturation of 88% with 6 L/min of oxygen via a Hudson mask. Chest radiograph showed bilateral lung infiltrates. Electrocardiography (ECG) revealed an inverted T waves in all the leads and this was further investigated with echocardiography (Echo) which revealed a normal chamber anatomy with global hypokinesia (basal > apical) with mid ventricular regional wall motion abnormalities (RWMA) and an ejection fraction of 30%. After admission to the intensive care unit, the patient complained of an occipital headache associated with rapid deterioration in the sensorium to a Glasgow coma score (GCS) of 6 (E2V2M2) following which the patient was intubated with rapid sequence intubation and mechanically ventilated on volume control mode. Post-intubation, computed tomography (CT) scan of the head showed a hematoma of the left cerebellar hemisphere caused due to a cerebellar arteriovenous malformation (AVM) causing herniation of the cerebellar tonsils. The lung status deteriorated progressively, wherein despite high FiO2 of 90% and PEEP of 12 the PaO2 was 58 mmHg and PaCO2 were 41 mmHg. The hemodynamic profile was unstable and systolic BP and mean arterial pressure (MAP) had to be maintained in the range of 120 mmHg and 60 mmHg with a combination of Inj. Dobutamine and Inj. Norepinephrine. The patient underwent conservative management for the cerebellar bleed as the relatives refused to give consent for surgical depression because of the high risk of perioperative mortality because of poor cardiopulmonary status and unstable hemodynamics. The patient was treated with head end elevation of 30 degrees, osmotherapy with 3% saline, hyperventilation to a target PaCO2 of 35 mmHg, Inj. Furosemide 20 mg and an Inj. Propofol infusion (50–100 mcg.kg −1.min −1) was started to provide neuroprotection and reduce intracranial pressure. Over 24 hours, the patient progressed to multi-organ dysfunction syndrome (MODS), i.e., a poor cardiac function requiring dual inotropic support, low lung compliance and inability to maintain oxygenation despite high FiO2 and PEEP and raised ICP resulting in tonsillar herniation and died 12 hours later.
Neurogenic stunned myocardium even though widely reported remains underappreciated due to its relatively unpredictable presentation and a lack of specific diagnostic markers. Various CNS disorders can result in NSM, but posterior fossa haemorrhage is not as common a cause as other cerebral pathologies such as traumatic brain injury, subarachnoid haemorrhage or seizures. Structural lesions of the cerebellum can cause mechanical compression of sub-lobular IX-b at the cerebellar uvula, dorsal reticular nucleus and A1 region in medulla oblongata resulting in a massive sympathetic discharge., Stimulation of these centres are the genesis for changes in both cardiovascular and respiratory functions. In our case, the sudden mechanical compression of the brainstem due to the cerebellar hemorrhage resulted in a massive sympathetic discharge causing a catecholamine surge resulting in NSM. The 'catecholamine hypothesis explains NSM', wherein the activation of the sympathetic nervous system results in catecholamine release from the sympathetic nerves innervating the myocardium. NSM presents as reduced ejection fraction and elevated cardiac enzymes in the absence of coronary artery disease or cardiac abnormalities., It is more appropriate to define NSM based on the decline in cardiac function, which can lead to hypotension and hypoxia. In NSM, the ischemic changes in ECG will be universally reflected in all leads and echocardiography will reveal global dyskinesia in NSM unlike myocardial infarction (MI) were the findings are restricted to a vascular territory. Although not performed in this patient, coronary artery disease is ideally ruled out with coronary angiography and resolution of cardiac stunning is confirmed with a repeated echocardiogram performed 2-4 weeks after the onset of NSM.
Clinical Presentation of NSM is similar to that of stress cardiomyopathy/Takotsubo cardiomyopathy which can also occur as a result of neurologic pathology as discussed by Baleine et al. in their case report of Takotsubo cardiomyopathy in a patient following cerebellar bleed. Both can have similar ECG presentation consisting of ST depression, T wave inversion and QT prolongation. Also, the cardiac troponins will be elevated in both the scenarios and both have cardiac dysfunction reversibility and pathologically have contraction band necrosis. The few marked differences are that NSM will be predisposed by an acute neurologic event, e.g. Subarachnoid/intracranial haemorrhage, traumatic brain injury, status epilepticus, whereas Takotsubo is a result of any physiological stress including acute neurogenic events. On echocardiography, NSM will have a basal compromise and mid-ventricular RWMA in contrast to Takotsubo which typically has apical compromise presenting as apical ballooning and mid-segmental RWMA's. NSM has a variable recovery rate of 66–78%, whereas Takotsubo has a better recovery profile of more than 92%. Takotsubo has a lower mortality rate (1-2%) but the mortality of NSM is variable depending on the pre-existing condition and the neurologic trigger.
In clinical practice, the goal of therapy of NSM is primarily focused on treating the underlying neurologic condition and reducing ICP in order to quell the sympathetic discharge responsible for causing multi-organ dysfunction. In contrast to the principles of brain resuscitation, where adequate tidal volume is the foundation stone, management of NSM may sometimes require a combination of protective ventilation with the prevention of hypoxemia and hypercapnia is required. Optimal oxygenation is achieved by using an adequate FiO2 and by application of appropriate PEEP to avoid the cerebral circulation getting affected by hemodynamic and CO2-mediated mechanisms. Ionodilators like milrinone, dobutamine and vasopressor therapy has been advocated for the treatment of the NSM. We opted for dobutamine as SBP <90 mmHg and dobutamine is found to be better than milrinone if the goal is to increase cardiac output in patients whose systemic vascular resistance (SVR) is low, and is hypotensive. Thus, any therapy of NSM must address the underlying cause resulting in catecholamine surge as well as manage the practical hemodynamic and cardiovascular realities which arise out of it.
Clinicians should have a high index of suspicion for neurogenic stunned myocardium while attending a case of acute onset cardiac failure especially in patients with no previous cardiac pathologies and associated neurological symptoms. Prompt diagnosis and management can reduce the incidence of mortality and morbidity in this subset of patients.
Consent obtained from the patient relative for publication of this case report.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their 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 their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
|1||Goncalves V, Silva-Carvalho L, Rocha I. Cerebellar haemorrhage as a cause of neurogenic pulmonary edema: A case report. Cerebellum 2005;4:246-9.|
|2||Ochiai H, Yamakawa Y, Kubota E. Deformation of the ventrolateral medulla oblongata by subarachnoid hemorrhage from ruptured vertebral artery aneurysms causes neurogenic pulmonary edema. Neurol Med Chir 2001;41:534-5.|
|3||Biso S, Wongrakpanich S, Agrawal A, Yadlapati S, Kishlyansky M, Figueredo V. A Review of neurogenic stunned myocardium. Cardiovasc Psychiatry Neurol 2017;2017:5842182.|
|4||Sugrue PA, Rengachary S, Guthikonda M. Neurogenic stunned myocardium: Mechanism and potential treatment modalities. Contemp Neurosurg 2007;29:1-7.|
|5||Baleine J, Jacquot A, Novais AR, Durand S, Milesi C, de la Villeon G, et al. Takotsubo cardiomyopathy in an adolescent girl. Arch Pediatr 2014;21:510-3.|
|6||Ripoll JG, Blackshear JL, Diaz-Gomez JL. Acute cardiac complications in critical brain disease. Neurosurg Clin N Am 2018;29:281-97.|