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A case of subarachnoid hemorrhage revealed by an acute coronary syndrome (ACS).

Hatim A, El Otmani W, Houssa MA, Atmani N, Moutakiallah Y, Haimeur C, Drissi M - Pan Afr Med J (2015)

Bottom Line: Surgical or endovascular treatment depends on location, size and shape of the aneurysm, on patient's age, neurological status and existence of concomitant diseases.We report the case of a 58 years old patient, with a past medical history of diabetes and hypertension, admitted for acute pulmonary edema with cardiogenic shock.This case illustrates an unusual presentation of aneurismal SAH in a patient presenting with an acute coronary syndrome.

View Article: PubMed Central - PubMed

Affiliation: Cardiovascular Surgery Department, Military Hospital Mohammed V, Rabat, Morocco.

ABSTRACT
The subarachnoid hemorrhage (SAH) is definitely the best descriptive model of the interaction between cardiovascular system and cerebral damage. The underlying mechanism of cardiovascular alterations after SAH is linked to the adrenergic discharge related to aneurysm rupture. Cardiac and pulmonary complications are common after severe brain injury, especially the aneurismal subarachnoid hemorrhage. Acute neurogenic pulmonary edema is not exceptional; it may occur in 20% of cases and commonly follows a severe subarachnoid hemorrhage. Severe myocardial damage with cardiogenic shock may possibly reveal the SAH (3% of cases) and mislead to wrong diagnosis of ACS with dramatic therapeutic consequences. The contribution of CT and cerebral angiography is essential for diagnosis and treatment. Surgical or endovascular treatment depends on location, size and shape of the aneurysm, on patient's age, neurological status and existence of concomitant diseases. We report the case of a 58 years old patient, with a past medical history of diabetes and hypertension, admitted for acute pulmonary edema with cardiogenic shock. This case illustrates an unusual presentation of aneurismal SAH in a patient presenting with an acute coronary syndrome.

No MeSH data available.


Related in: MedlinePlus

(A) MRA: angiographic embolization with microspheres of the aneurysm; (B): postembolization angiography
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Figure 0002: (A) MRA: angiographic embolization with microspheres of the aneurysm; (B): postembolization angiography

Mentions: A 58-year-old man with a past medical history of poorly controlled hypertension and type 2 diabetes, presented to the ICU for a cardiogenic shock complicating acute myocardial infarction. Physical examination revealed reduced level of consciousness (Glasgow Coma Scale 10/15) and weak vital signs; a blood pressure of 80/50 mmHg, 80% of oxygen saturation, capillary blood glucose at 2.26 g/L, a heart rate over 125 bpm, and crackling in pulmonary auscultation. Cardiovascular examination showed neither cardiac murmur nor signs of right heart failure. ECG on admission showed normal sinus rhythm, with heart rate of 125 bpm and extended ST-elevation in anterior territory. Laboratory results demonstrated Troponin I level of 6.41 ng/ml, creatinine kinase (CKMB) was 67 UI/L, Lactate deshydrogenase was 281 UI/L, glucose level 2.70 g/l, urea 0.40 g/l and creatinine 18.6 mg / L. The patient was intubated and sedated, inotropic agents were started (norepinephrine 0.4µg/kg/min and dobutamine 20µg/kg/min). Chest X-rays showed diffuse alveolar syndrome. Transthoracic echocardiography revealed wall motion abnormalities namely extensive akinesis of anteroseptal, anterior, lateral and inferior walls, and severe left ventricular systolic dysfunction (ejection fraction of 29%). Medical management was initiated; anticoagulant therapy for acute coronary syndrome was started (500 mg of acetylsalicylic acid and subcutaneous low-molecular-weight heparin (0.6ml of enoxaparin)) and patient was prepared for myocardial revascularization by coronary angioplasty. Because of non-improvement of neurological status and occurrence of seizures, a brain CT was indicated and revealed infratentorial diffuse hemorrhage (Fisher grade III) (Figure 1). Cerebral angiography confirmed a dissecting aneurysm of an anastomotic branch between left PICA and the V4 segment of left vertebral artery Figure 2 that was successfully embolized. After 24 hours, the patient improved with withdrawal of vasoactive drugs in 24 hours. Left hemicorporeal seizures persisted despite anticonvulsant treatment. Control brain CT did not report rebleeding and angiography showed complete exclusion of the aneurysm while the EEG revealed a diffuse brain damage. 10 days after admission, the patient was discharged in stable condition but still suffers from amnesia.


A case of subarachnoid hemorrhage revealed by an acute coronary syndrome (ACS).

Hatim A, El Otmani W, Houssa MA, Atmani N, Moutakiallah Y, Haimeur C, Drissi M - Pan Afr Med J (2015)

(A) MRA: angiographic embolization with microspheres of the aneurysm; (B): postembolization angiography
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4537903&req=5

Figure 0002: (A) MRA: angiographic embolization with microspheres of the aneurysm; (B): postembolization angiography
Mentions: A 58-year-old man with a past medical history of poorly controlled hypertension and type 2 diabetes, presented to the ICU for a cardiogenic shock complicating acute myocardial infarction. Physical examination revealed reduced level of consciousness (Glasgow Coma Scale 10/15) and weak vital signs; a blood pressure of 80/50 mmHg, 80% of oxygen saturation, capillary blood glucose at 2.26 g/L, a heart rate over 125 bpm, and crackling in pulmonary auscultation. Cardiovascular examination showed neither cardiac murmur nor signs of right heart failure. ECG on admission showed normal sinus rhythm, with heart rate of 125 bpm and extended ST-elevation in anterior territory. Laboratory results demonstrated Troponin I level of 6.41 ng/ml, creatinine kinase (CKMB) was 67 UI/L, Lactate deshydrogenase was 281 UI/L, glucose level 2.70 g/l, urea 0.40 g/l and creatinine 18.6 mg / L. The patient was intubated and sedated, inotropic agents were started (norepinephrine 0.4µg/kg/min and dobutamine 20µg/kg/min). Chest X-rays showed diffuse alveolar syndrome. Transthoracic echocardiography revealed wall motion abnormalities namely extensive akinesis of anteroseptal, anterior, lateral and inferior walls, and severe left ventricular systolic dysfunction (ejection fraction of 29%). Medical management was initiated; anticoagulant therapy for acute coronary syndrome was started (500 mg of acetylsalicylic acid and subcutaneous low-molecular-weight heparin (0.6ml of enoxaparin)) and patient was prepared for myocardial revascularization by coronary angioplasty. Because of non-improvement of neurological status and occurrence of seizures, a brain CT was indicated and revealed infratentorial diffuse hemorrhage (Fisher grade III) (Figure 1). Cerebral angiography confirmed a dissecting aneurysm of an anastomotic branch between left PICA and the V4 segment of left vertebral artery Figure 2 that was successfully embolized. After 24 hours, the patient improved with withdrawal of vasoactive drugs in 24 hours. Left hemicorporeal seizures persisted despite anticonvulsant treatment. Control brain CT did not report rebleeding and angiography showed complete exclusion of the aneurysm while the EEG revealed a diffuse brain damage. 10 days after admission, the patient was discharged in stable condition but still suffers from amnesia.

Bottom Line: Surgical or endovascular treatment depends on location, size and shape of the aneurysm, on patient's age, neurological status and existence of concomitant diseases.We report the case of a 58 years old patient, with a past medical history of diabetes and hypertension, admitted for acute pulmonary edema with cardiogenic shock.This case illustrates an unusual presentation of aneurismal SAH in a patient presenting with an acute coronary syndrome.

View Article: PubMed Central - PubMed

Affiliation: Cardiovascular Surgery Department, Military Hospital Mohammed V, Rabat, Morocco.

ABSTRACT
The subarachnoid hemorrhage (SAH) is definitely the best descriptive model of the interaction between cardiovascular system and cerebral damage. The underlying mechanism of cardiovascular alterations after SAH is linked to the adrenergic discharge related to aneurysm rupture. Cardiac and pulmonary complications are common after severe brain injury, especially the aneurismal subarachnoid hemorrhage. Acute neurogenic pulmonary edema is not exceptional; it may occur in 20% of cases and commonly follows a severe subarachnoid hemorrhage. Severe myocardial damage with cardiogenic shock may possibly reveal the SAH (3% of cases) and mislead to wrong diagnosis of ACS with dramatic therapeutic consequences. The contribution of CT and cerebral angiography is essential for diagnosis and treatment. Surgical or endovascular treatment depends on location, size and shape of the aneurysm, on patient's age, neurological status and existence of concomitant diseases. We report the case of a 58 years old patient, with a past medical history of diabetes and hypertension, admitted for acute pulmonary edema with cardiogenic shock. This case illustrates an unusual presentation of aneurismal SAH in a patient presenting with an acute coronary syndrome.

No MeSH data available.


Related in: MedlinePlus