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Value of triple H therapy in a patient with an ischemic penumbra following subarachnoid hemorrage: a case study.

Abstract: We report the case of a 43-year-old patient with delayed ischemic neurological deficit and an ischemic penumbra, reversed with triple H therapy (hypertension, hypervolemia, and hemodilution). The patient presented with subarachnoid hemorrhage caused by an aneurysm of the anterior communicating artery. He underwent surgical clipping and developed cerebral ischemia due to vasospasm. Permanent damage to the area of ischemic brain was prevented by institution of the triple H therapy. He recovered and was discharged with no subsequent neurological deficits.


A patient admitted to the local general hospital had been found collapsed in his bathroom. He had no recollection of what had happened or how long he may have been in the bathroom. He complained of having a headache and neck pain and vomiting. Clinical evaluation revealed bleeding from the nose and no other evidence of a head injury. His Glasgow Coma Scale (GCS; Teasdale and Jennett, 1974) score was 15, and he had normal cardiorespiratory parameters. Plain skull x rays were normal with no vault fractures noted. He was admitted for observation. A computed tomography (CT) scan of the brain was not performed initially because he was suspected to have a mild head injury. Twenty-four hours later, his headache was no better. A CT scan of the brain was ordered. This revealed a subarachnoid hemorrhage (SAH) with early hydrocephalus (Fig 1). He was transferred to the neurosurgical unit.


On admission to the unit, he had a GCS score of 15 and a World Federation of Neurological Societies (WFNS) grade 1 SAH (Teasdale et al., 1988; Ogungbo, 2003). He was agitated and had severe headaches, photophobia, neck-stiffness, and a mild left-sided pronator drift. We commenced routine therapy with nimodipine (Bayer, UK), fluid replacement, steroids (dexamethasone) for headache management, and sodium valproate (Epilim, Sanofi-synthelabo, UK) prophylaxis for seizure.

Three days following admission, he was stable enough to undergo angiography. This revealed a small, saccular, wide-necked aneurysm of the anterior communicating artery complex. There was evidence of vasospasm in the anterior cerebral arteries bilaterally. The aneurysm was considered unsuitable for coiling, and so a craniotomy and clipping were performed the next day, 5 days following his collapse. The operation, via a left pterional and gyrus rectus approach, went well, and his early recovery was satisfactory

On day 8 from the ictus and 3 days following the operation, his nurse noted that he was confused and had mild weakness of the right arm. His blood pressure (BP) averaged 140/70 mm Hg with a pulse rate of 60 beats per minute. ACT scan of the brain (Fig 2) showed a hypodense area in the left head caudate and anterior limb of the internal capsule. We performed transcranial Doppler (TCD) measurements (Fig 3). Routine hematological and biochemistry tests were satisfactory with normal hematocrit and serum sodium. He was laid flat to improve cerebral blood flow and started on hypervolemic and hypertensive therapy with hemodilution (triple H therapy). Triple H therapy improves cerebral circulation by reducing viscosity, improving flow, and increasing the delivery of blood to ischemic brain tissue. Hypertension was induced with titrated noradrenaline infusion to maintain the BP at above 160 mm Hg. Arterial and central venous pressure (CVP) lines were inserted and the parameters (BP > 160 mm Hg, CVP = 10-12 cm[H.sub.2]O) maintained rigorously for 11 days. Expert nursing care was vital in the management of this patient. He required critical monitoring, strict fluid balance, and early detection and correction of biochemical anomalies, especially sodium balance. Clinically he improved, and treatment was discontinued on the 17th day Repeat CT (Fig 4) scan demonstrated resolution of the area of low density previously reported.



The patient had SAH, which was initially misdiagnosed as a head injury. However, because his clinical condition failed to improve after 24 hours, a CT scan of the brain was ordered to evaluate the continued complaint of severe headache. This revealed extensive SAH, and he was referred for neurosurgical management. Patients with SAH are considered for admission in our unit on the basis of their clinical condition and physiological age. We evaluate the patients to confirm the diagnosis, determine the cause via angiography, and incorporate early embolization/surgery in suitable patients. The protocol for patient management (WFNS grades I and 2) involves early confirmatory angiography and clipping or coiling of aneurysm(s) at the earliest opportunity (Ogungbo et al., 2001). Poor grade patients (WFNS grades 4-5) are accepted for management of raised intracranial pressure, intensive care, and consideration for endovascular treatment. However, treatment is often delayed until their clinical conditions improve. Medical treatment of some of the patients includes a short course of dexamethasone (4 mg, 4 times daffy) or severe headaches. Dexamethasone is used in addition to normal analgesics prescribed for headaches; this has been found to be beneficial without causing any additional complications (Schurkamper, Medele, Zausinger, Schmid-Elsaesser, & Steiger, 2004).

The SAH in this patient was caused by an aneurysm of the anterior communicating artery, which was surgically treated. Postoperatively, hydrocephalus, hyponatremia, and cerebral ischemia are recognized complications in patients with SAH. Rational treatment requires individual causes of neurological deterioration to be identified early and treatment to be targeted at the mechanism. There was evidence of vasospasm of the anterior cerebral artery complex, and he deteriorated clinically with evidence of symptomatic delayed ischemic neurological deficit (DIND) 3 days after surgery (8 days after SAH). An area of low density seen on the CT scan of the brain represented impending cerebral infarction in the head of caudate on the left (Fig 2). This corresponds to the area of supply by the artery of Heubner (left), a branch of the anterior cerebral artery.

The TCD measurements also showed high pressures in the middle cerebral arteries. The TCD pressures of the anterior cerebral arteries were difficult to obtain probably due to severe spasm. It has been shown that TCD conducted at different phases of SAH can not only demonstrate the functional and pathological status of cerebral blood vessels following SAH, but also reflect the clinical outcome (Jiang, Shi, & Gao, 1999). A TCD mean velocity threshold of 160 cm/sec accurately detects clinical vasospasm (Mascia et al., 2003). Measures of proven value in decreasing the risk of DIND are a liberal supply of fluids, avoidance of antihypertensive drugs, and administration of nimodipine. Once ischemia has occurred, treatment regimens such as a combination of induced hypertension and hypervolemia, or transluminal angioplasty, are plausible but of unproven benefit (van Gijn & Rinkel, 2001). This patient had evidence of clinical and radiological vasospasm. The patient was treated flat with complete bed rest, fluid therapy (minimum of 3 liters of a combination of saline and volume expanders per day), nimodipine, and noradrenaline as previously detailed. This led to prevention of a stroke in evolution and a resolution of the area of impending infarction (penumbra) on the CT scan of the brain (Fig 4).

Acute treatment of stroke aims to preserve the ischemic penumbra, protect neurons against further ischemia and enhance brain plasticity to maximize recovery. It is extremely important to distinguish the penumbra from the ischemic core in focal cerebral ischemia, because the penumbra contains viable tissue, which can be salvaged by appropriate treatment (Liu et al., 2003). It is even more important to apply treatment in a timely fashion because triple H therapy can worsen brain edema in the presence of acute infarction and hence is contraindicated in some patients (Gupta, Sharma, Gupta, Bapuraj, & Khosla, 2000).

Close nursing observations and care in the high-dependency unit enabled early detection of the deterioration. The patient had a good recovery mainly because the deteriorating situation was reversed by salvage of the penumbra and limiting the area of core brain damage. He was discharged home with complete recovery and no obvious physical or neuropsychological deficits.


Hemodynamic (BP, CVP, TCD) and biochemical (serum sodium and potassium) monitoring is crucial in the management of patients with SAH. Triple H therapy is useful in treating delayed ischemic neurological deficit caused by the ischemic penumbra. It should be started early, and the value of the individual components of therapy should be reviewed regularly.


Gupta, D., Sharma, B. S., Gupta, S. K., Bapuraj, R., & Khosla, V. K. (2000). Postoperative hypertensive-hypervolaemic-haemodilution (Triple H) therapy in the treatment of vasospasm following aneurysmal subarachnoid hemorrhage. Neurology India, 48, 126-131.

Jiang, Y., Shi, Q., & Gao, Q. (1999). Application of transcranial Doppler in subarachnoid hemorrhage. Journal of Tongji Medical University, 19, 230-232.

Liu, S., Liu, M., Peterson, S., Miyake, M.,Vallyathan, V., & Liu, K.J. (2003). Hydroxyl radical formation is greater in striatal core than in penumbra in a rat model of ischemic stroke. Journal of Neuroscience Research, 71, 882-888.

Mascia, L., Fedorko, L., terBrugge, K., Filippini, C., Pizzio, M., Ranieri, V. M., et al. (2003).The accuracy of transcranial Doppler to detect vasospasm in patients with aneurysmal subarachnoid hemorrhage. Intensive Care Medicine, 29, 1088-1094.

Ogungbo, B. (2003). The World Federation of Neurological Surgeons scale for subarachnoid hemorrhage. Surgical Neurology, 59, 236237; discussion 237-238.

Ogungbo, B., Gregson, B.A., Blackburn,A, Mendelow, A. D., & Newcastle Subarachnoid Study Group. (2001).Trends over time in the management of subarachnoid hemorrhage in Newcastle: Review of 1609 patients. British Journal of Neurosurgery, 15, 388-395.

Schurkamper, M., Medele, R., Zausinger, S., Schmid-Elsaesser, R., & Steiger, H. J. (2004). Dexamethasone in the treatment of subarachnoid hemorrhage revisited: A comparative analysis of the effect of the total dose on complications and outcome.Journal of Clinical Neuroscience, 11, 20-24.

Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness.A practical scale. Lancet, 2, 81-84.

Teasdale, G. M., Drake, C. G., Hunt, W, Kassell, N., Sano, K., Pertuiset, B., et al. (1988). A universal subarachnoid hemorrhage scale: Report of a committee of the World Federation of Neurosurgical Societies. Journal of Neurology, Neurosurgery, and Psychiatry, 51, 1457.

van Gijn, J., & Rinkel, G.J. (2001). Subarachnoid hemorrhage:Diagnosis, causes and management. Brain, 124, 249-278.

Questions or comments about this article may be directed to Biodun Ogungbo, MBBS FRCS MSc, by telephone at 01642850850 or by e-mail message at He is a specialist registrar in neurosurgery, at James Cook University Hospital, Middlesbrough, United Kingdom.

Savithru Prakash, MBBS, is a senior house officer in neurosurgery at James Cook University Hospital, Middlesbrough, United Kingdom.

Shungu Ushewokunze, MBBS FRCS, is a senior house officer in neurosurgery at James Cook University Hospital, Middlesbrough, United Kingdom.

Kevin Etherson, MB ChB, is a senior house officer in neurosurgery at James Cook University Hospital, Middlesbrough, United Kingdom.

John Sinar, MBBS FRCS, is a consultant neurosurgeon at James Cook University Hospital, Middlesbrough, United Kingdom.
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Title Annotation:care and treatment of subarachnoid hemorrage
Author:Ogungbo, Biodun; Prakash, Savithru; Ushewokunze, Shungu; Etherson, Kevin; Sinar, John
Publication:Journal of Neuroscience Nursing
Geographic Code:1USA
Date:Dec 1, 2005
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