Update on the Management of Subarachnoid Hemorrhage - Page 7 (2024)

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Future Neurology

Katja E Wartenberg

Disclosures

Future Neurology.2013;8(2):205-224.

Update on the Management of Subarachnoid Hemorrhage - Page 7 (1)

In This Article

  • Abstract and Introduction
  • Aneurysm Repair
  • Delayed Cerebral Ischemia
  • Prevention of DCI
  • Electrolyte Disturbances
  • Treatment of Medical Complications
  • Prognosis
  • Conclusion
  • Future Perspective
  • References
  • Sidebar

Electrolyte Disturbances

Hyponatremia occurs in 20–40% of SAH patients. Hypomagnesemia (40%), hypokalemia (25%) and hypernatremia (20%) are also common after SAH.[156–159] Hyponatremia is usually caused by inappropriate secretion of antidiuretic hormone and free-water retention and/or excessive renal sodium excretion due to increased atrial natriuretic factor, so called 'cerebral salt wasting syndrome'.[159,160] Intravascular volume depletion and sodium loss may increase the risk of DCI and infarction.[84,85] In 124 WFNS grade IV and V patients, hyponatremia (serum sodium <135 mmol/l) developed in 63% of patients, caused by cerebral salt wasting syndrome in 55%. Late-onset hyponatremia (between SAH day 4 and 9) correlated with a higher occurrence of cerebral infarction in this patient population. Nevertheless, hyponatremia did not have an association with poor outcome at 3 months (Glasgow Outcome Scale: 1–3).[161]

Fludrocortisone and hydrocortisone were studied for the prevention of hyponatremia in SAH.[162–166] If started early, the corticosteroids are effective in the prevention of natriuresis and hyponatremia. However, their use was complicated by hyperglycemia and hypokalemia.

Administration of large-volume isotonic crystalloids and restriction of free-water intake should be applied to counteract potential hypovolemia and to prevent inappropriate water retention. Hypertonic saline (3%) may be used to correct hyponatremia.[56,167]

Conivaptan is an arginine vasopressin receptor antagonist (V1A/V2) approved for the treatment of euvolemic and hypervolemic hyponatremia.[168] Initial reports of its use in neurocritical care patients with hyponatremia have yielded promising results.[169] Caution should be taken to avoid hypovolemia with the use of conivaptan.[56]

1 2 3 4 5 6 7 8 9 10 11

Next Section

Future Neurology.2013;8(2):205-224.©2013 Future Medicine Ltd.

  • Abstract and Introduction
  • Aneurysm Repair
  • Delayed Cerebral Ischemia
  • Prevention of DCI
  • Electrolyte Disturbances
  • Treatment of Medical Complications
  • Prognosis
  • Conclusion
  • Future Perspective
  • References
  • Sidebar
Tables
Table 1. Acute management and resuscitation goals of subarachnoid hemorrhage.
Aspect of care Management
Blood pressure Invasive monitoring
Goal: systolic <160 mmHg, diastolic <110 mmHg and mean blood pressure <110 mmHg, CPP >60 mmHg until aneurysm repair
Drugs: iv. urapidil 5–40 mg/h, iv. labetalol 5–150 mg/h, iv. nicardipine 5–15 mg/h, iv. clevidipine 1–32 mg/h, iv. esmolol 50–100 µg/kg/min, iv. metoprolol 1–5 mg/h, iv. hydralazine 1.5–7.5 mg/h, iv. clonidine 0.03–0.12 mg/h
Prevention of rebleeding Aneurysm repair through coiling or clipping
Option: ε-aminocaproic acid 4 g iv., followed by 1 g/h for a maximum of 72 h, up to 4 h prior to angiogram
Fluid balance Monitoring through cardiac output monitor measuring stroke volume variation (most accurate, only in fully mechanically ventilated patients), internal jugular or subclavian central line (CVP – less reliable), urine output and clinically
Isotonic fluids for fluid replacement only: 0.9% NaCl at 1.0–1.5 ml/kg/h
Oxygenation Goal: oxygen saturation >90%
Intubation and mechanical ventilation if GCS <8
Fever control Goal: temperature ≤37°C
Methods: iv. or p.o. acetaminophen or metamizol 500–1000 mg, if not successful: ice packs, cold wraps, surface or endovascular temperature control systems with management of shivering
Glucose control Goal: 4.5–7.0 mmol/l (81–126 mg/dl)
Methods: continuous insulin infusion
Caution: avoid hypoglycemia
Option: adjust to cerebral glucose level if microdialysis is used
Nutrition Enteral nutrition should be started and be at goal (25–30 kcal/kg/day) within 48 h of admission
DVT prophylaxis Sequential compression devices
Heparin 5000 units sc. every 8 h or enoxaparin 30–40 mg sc. daily within 24 h after aneurysm repair, withhold 24 h before and after intracranial procedures
Aspiration prophylaxis Head-of-bed elevation 30°
Gastric protection Pantoprazole 20–40 mg iv. or p.o. daily
Laboratory Admission: electrolytes, CBC, coagulation, d-dimer, troponin I, creatine kinase, type and cross blood, urine analysis and toxicology screening
Daily: CBC, electrolytes, creatinine and blood gas
Other tests ECG
Chest radiograph
Option: transthoracic echocardiography
Hyponatremia Isotonic fluids: 0.9% NaCl at 1.0–1.5 ml/kg/h
Limit free-water intake
Options: 2–20% hypertonic saline solutions, NaCl tablets and fludrocortisone or hydrocortisone for negative fluid balance
Seizure prophylaxis Anti-epileptic treatment for patients with initial seizure, focal intracerebral clot or focal cerebral edema prior to aneurysm clipping with levetiracetam 500–2000 mg iv. daily divided into two dosages
Maximum 3–7 days without evidence of seizures
Electroencephalography monitoring of patients with Hunt and Hess grade IV and V
Extraventricular drainage Emergent EVD placement for all patients with Hunt and Hess grade IV and V, decreased mental status and hydrocephalus
Raising the EVD level or clamping dependent on EVD output as soon as possible
No antibiotic prophylaxis
CSF for cell count and differential, glucose, lactate and protein every other day; culture if cell count increases
Caution: many CSF drawings increase the risk of infections. Sterile conditions should be applied
Neurogenic stunned myocardium with pulmonary edema Hemodynamic monitoring (PiCCO, Pulsion Medical Systems, Munich, Germany; Flo Trac, Edwards Lifesciences, Irvine, CA, USA; pulmonary artery catheter)
Goal MAP: 70–90 mmHg
Inotropic support: milrinone 0.25–20.75 µg/kg/min or dobutamine 3–15 µg/kg/min
Vasopressors: norepinephrine 0.03–00.6 µg/kg/min (first choice), phenylephrine 2–10 µg/kg/min or dopamine 5–30 µg/kg/min
Diuresis
Increase FiO2 and PEEP
Transthoracic echocardiography
Vasospasm prophylaxis and diagnosis Nimodipine 60 mg p.o. every 4 h until SAH day 21
Option: simvastatin 40–80 mg p.o. or pravastatin 40 mg p.o. daily until SAH day 14
Avoid hypomagnesemia
Daily transcranial Doppler sonography including the Lindegaard index
Option: CT angiography, CT perfusion or MR perfusion imaging on SAH day 4–12 (mean 9) in high-risk patients (Hunt and Hess grade IV and V; modified Fisher grade III and IV)
Vasospasm therapy Consider Trendelenburg position (head down)
Caution: increased rates of ventilator-associated pneumonia
Infusion of 500–1000 ml 0.9% saline or 5% albumin over 15 min
Start vasopressors (norepinephrine, phenylephrine or dopamine) to raise systolic blood pressure to 160–220 mmHg (20 mmHg above current) until deficits resolve
Consider milrinone or dobutamine in patients with congestive heart failure or myocardial ischemia
Refractory vasospasm
• Angiographic angioplasty and/or intra-arterial papaverine, verapamil or nicardipine
• Hemodynamic monitoring with PiCCO or Flo Trac, augmentation for goal cardiac index ≥4.0 l/min/m2 and diastolic pulmonary artery pressure >14 mmHg with dobutamine or milrinone

CBC: Complete blood count; CPP: Cerebral perfusion pressure; CSF: Cerebrospinal fluid; CT: Computed tomography; CVP: Central venous pressure; DVT: Deep vein thrombosis; EVD: Extraventricular drainage; FiO2: Inspired fraction of oxygen; GCS: Glasgow Coma Scale; iv.: Intravenous; MAP: Mean arterial pressure, MR:Magnetic resonance tomography; NaCl: Sodium chloride; PEEP: Positive endexpiratory pressure; PiCCO: Pulse contour cardiac output monitoring; p.o.: By mouth; SAH: Subarachnoid hemorrhage; sc.:Subcutaneously.
Reproduced with permission from Oxford University Press, NY, USA.219

References
Authors and Disclosures

Authors and Disclosures

Katja E Wartenberg

Neurocritical Care Unit, Department of Neurology, Martin-Luther-University Halle-Wittenberg, Ernst-Grube-Strasse 40, 06120 Halle (Saale), Germany. katja.wartenberg@medizin.uni-halle.de

Financial & competing interests disclosure
The author has no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.

Sidebar

Sidebar

Executive Summary

Clinical Presentation & Diagnosis

  • Thunderclap headache, followed by nausea and vomiting, is the typical feature of subarachnoid hemorrhage (SAH).

  • The sensitivity of SAH detection by computed tomography approaches 100% within the first 6 h.

  • Cerebral angiography remains the gold standard to demonstrate the ruptured aneurysm, although computed tomography angiography can detect aneurysms with comparable sensitivity.

  • The modified Fisher scale provides a more accurate prediction of the probability of vasospasm.

General Emergency & Critical Care Management

  • Emergency management should focus on the restoration of airway, breathing and circulation with attention to blood pressure and seizure control and the treatment of intracranial hypertension.

  • An external ventricular drain is indicated for the emergency management of hydrocephalus and monitoring of intracranial pressure. Up to 26% of patients require a ventriculoperitoneal shunt.

  • Multimodal monitoring may help to determine the optimal cerebral perfusion pressure threshold.

  • Euvolemia is the target for volume status.

  • The patients diagnosed with SAH should be treated at high-volume centers (>35 cases per year).

Aneurysm Repair

  • The treatment modalities coiling and clipping depend on the clinical condition of the patient and the anatomy of the aneurysm.

  • A case discussion among experts should determine the appropriate treatment modality and the patient should be treated in a specialized neurointensive care unit.

Delayed Cerebral Ischemia

  • Monitoring for delayed cerebral ischemia with frequent neurological exams and/or transcranial Doppler sonography is mandatory in good-grade patients. A change in clinical examinations or an increase in mean flow velocities >200 cm/s or in the Lindegaard ratio >6 should trigger a vascular imaging study. A clinical examination in an awake patient is often more helpful, as the sensitivity of the diagnosis of vasospasm by transcranial Doppler sonography is rather low.

  • Poor-grade patients require different monitoring techniques in addition to transcranial Doppler sonography

  • Medical treatment of delayed cerebral ischemia consists of induced hypertension and/or augmentation of cardiac output. Balloon angioplasty and intra-arterial vasodilators are endovascular treatment options.

Electrolyte Disturbances

  • Hyponatremia, hypomagnesemia, hypokalemia and hypernatremia are also common after SAH and should be corrected.

Treatment of Medical Complications

  • Intensive care management should target normothermia and normoglycemia avoiding hypoglycemia, treatment of myocardial dysfunction and pulmonary edema.

Prognosis

  • With further reduction of mortality by improved repair techniques and critical care management, the long-term outcome after SAH has improved, especially in poor-grade patients.

  • Older age, poor clinical grade upon presentation, rebleeding, larger aneurysm size, global cerebral edema, delayed cerebral ischemia and medical complications impact functional outcome after SAH.

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