EMCrit.org

SubArachnoid Hemorrhage

Causes

trauma most common

rupture of saccular (berry) aneurysm most common nontraumatic cause: 80%.  85% in anterior circulation.

20% have ruptured arteriovenous malformation (AVM)

perimesencephalic hemorrhages

Symptoms

Can be the worst HA ever, but can also be a HA of a new type for the patient.  N/V makes SAH more likely.  Syncope or neurological findings merit suspicion.  Very worrisome is a HA that has it's onset in <1 minute, usually <10 seconds (thunderclap) 1 in 5 will have SAH

Takes 6-12 hours for meningeal signs to develop. 40% have no localizing signs. (J Neurol 243:p. 496, 1996)

Risk factors:  vascular disease; family history of SAH (4 times higher risk); prior SAH (6 times higher risk)

Evaluation 

Evaluate for severity, onset, quality and assoc. symptoms (n/v, diplopia, syncope, seizures)

Signs are nuchal rigidity, neuro findings (esp. 3^rd nerve palsy), retinal or vitreous bleeding)

CT

first 95% sensitivity which declines with time from injury. Maximum sensitivity at less than 12 hours.  Anemic patients also decrease sensitivity

recent analysis of sensitivity is 93% (88-97) (Ann Emerg Med 2008;51:697)

Ask for thin cuts through base of brain (3mm)

Most studies evaluating the sensitivity of CT scan in SAH have problems with spectrum bias, ? of what a positive reading is (some say a + reading is if 1 of 3 neuroradiologists saw the bleed,) creiterion standards, etc. (Annals of EM 37:3, 2001)

False-negative CT can be caused by hemoglobin count <10 mg/dL (blood isodense with brain, making it impossible to detect); overall sensitivity of new-generation CT 91% to 93%; timing important (sensitivity best within first 12 hr)

Figure 3. CT scan results for SAH and the confirmed outcomes (if SAH was actually present or not).

(Boesiger Journal of Emergency Medicine
Volume 29, Issue 1, July 2005, Pages 23-27)

LP

SAH has been reported with just a few hundred cells.

Initially the WBCs will be in 1:700 ratio  with RBCs, as time passes inflammatory response will lead to increased PMNs (3-5 days)

2/3’s of SAH will have elevated opening pressure, do not need to unbend legs, might as well unbend head.

Very difficult to differentiate a traumatic tap from SAH.  3 tube clearing method doesn’t work (J Neur Neurosurg Psych 1981:44), numerous reasons included layering and the possibility of coincident SAH and traumatic tap.  Probably best to just consider the last tube as the true cell count.

Xanthrochromia is reliably present from 12 hours to 2 weeks (J Neurol 243: p. 496, 1996)

We are not sensitive when we try to figure it out visually (Xanthrochromia: By Which Method? A Comparison of the Visual
and Spectrophotometric Determination of Xanthrochromia Annals EM Oct 2004 44:4)

If xanthochromia is read by machine, may need to wait 12 hrs to do LP.  Do not need to wait if read by eye, but can mistake the pink from newly lysed cells (oxyhemoglobin) in traumatic tap with true yellow of degraded cell contents (billirubin, which is never present in traumatic taps.)  

Xanthrochromia is not pathognomonic for SAH if tubes wait more than two hours before being analyzed by eye, 2° to above (Acad EM May 2002 9:5, 412)

or unfortunately by spectrophotometry:  xanthrochromia was present in nontraumatic samples within two hours if the traumatic tap was >10,000 reds, immediately with >30,000 and one hour with >20,000 (Acad Emerg Med Feb 2004, 11:2 p. 131)

(J EM 23:1 2002)

In 1 study of thunderclap headaches with proven SAH, 1 in 5 had a negative CT with a positive LP. (Cephalgia 22:354, June 2002)

visual inspection is insensitive for xanthrochromia (annals of em 2005;46:1)

Figure 6. Xanthochromia of cerebrospinal fluid

Haemorrhagic cerebrospinal fluid after centrifugation shows a yellow colour (right) compared with water (left), which proves that blood was not introduced during puncture.

Clear cerebrospinal fluid should also be sent for culture, because meningitis, especially pneumococcal meningitis, can present acutely. If the cerebrospinal fluid is blood-stained, it should be spun down immediately. If the supernatant is yellow (compared with water against a white background), the diagnosis of subarachnoid haemorrhage is practically certain (figure 6), though formally the presence of bilirubin needs to be established. Bilirubin can be formed only in vivo, whereas haemoglobin can also be broken down to oxyhaemoglobin, in a test tube that has been left unattended before it was spun down. The specimen should be stored in darkness, preferably wrapped in tinfoil because the ultraviolet components of daylight can break down bilirubin—not only in icteric newborn babies, but also in test tubes. Spectrophotometry can not only confirm the presence of bilirubin but also exclude it,⁵¹ although experienced neurologists and neurosurgeons can confidently exclude xanthochromia by visual inspection alone.⁵²

Treatment

Use Labetolol or cardene

Give nimodipine 60 mg PO/NGT Q4

Load dilantin and keep pt slightly hypervolemic to attenuate vasospasm.

BP SBP<140 (160) and MAP<100 until aneurysm secured

Hunt and Hess Classification
Grade 1 – Asymptomatic, or minimal headache and slight nuchal rigidity
Grade 2 – Moderate to severe headache, nuchal rigidity; no neurological deficit other than cranial nerve palsy
Grade 3 – Drowsiness, confusion, or mild focal deficit
Grade 4 – Stupor, moderate to severe hemiparesis, possible early decerebrate rigidity and vegetative disturbances
Grade 5 – Deep coma, decerebrate rigidity, moribund appearance

Perimesencephalic hemorrhage:  will have negative angiogram.  No risk of rebleeding or ischemic consequence.

(Review:  JB24-NEJM 342:1,

Small warning leaks (sentinel bleeds): patients look well and usually have normal physical examination; difficult to decide whether workup indicated; sentinel bleeds can produce focal or diffuse headache that can be minor or severe (usually precedes rupture by hours to months, average 2 wk); differential diagnosis includes leak, expansion, dissection, or thrombosis of unruptured aneurysm; usually do not cause increased intracranial pressure or meningeal irritation; important to pick up leaks, because 65% of patients rebleed and worsen (peak incidence in 2-7 days)

More on aneurysms: dizziness can be sign of growing aneurysm; posterior communicating artery aneurysm can cause progressively worsening retro-orbital headache and oculomotor nerve palsy; middle cerebral artery aneurysm can cause stroke-like symptoms in upper extremities; anterior communicating artery aneurysms usually cause stroke-like leg symptoms; basilar artery aneurysms can cause vertical gaze and coma; patient with aneurysm in posterior circulation can present with vertigo alone; aneurysms also can develop thrombus and throw clots, causing transient ischemic attack (TIA)

Conditions confused with SAH: viral meningitis, migraine, sinusitis, sinus headache, stroke, hypertension, tension headache, neck arthritis or strain, depression, back pain, altered mental status

Case 4: man falls off ladder; CT shows subarachnoid blood; wife says husband grabbed his head before he fell off ladder

SAH in head-injured patient: common cause of confusion; subarachnoid blood assumed due to trauma; consider ruptured aneurysm whenever focal subarachnoid blood seen in sylvian fissure, interhemispheric fissure, or basal cisterns

Electrocardiographic (ECG) changes: fairly common in patients with SAH; 20% look ischemic; may see nonspecific T wave changes, prolonged QRS, U waves, increased QT intervals; approximately 91% of patients have arrhythmias sometime during course of SAH

Complications after rupture: delayed cerebral ischemia from vasospasm (in 20%); hydrocephalus (blood in ventricle inhibits flow of cerebrospinal fluid [CSF]); severe headache; altered mental status; incidence and mortality have remained unchanged despite advances in detection and treatment

Magnetic resonance imaging: greater sensitivity in subacute and chronic cases; can detect aneurysms >3 mm and determine if aneurysm contains thrombus

Magnetic resonance angiography (MRA): sensitivity 95%; technology rapidly improving; may eventually replace angiography; helpful in detecting whether patient bleeding from AVM; may not detect posterior and anterior communicating artery aneurysms

we would use full dose (enteral) nimodipine and betablocker
(we use metoprolol)for hypertension and get a sedative-free CNS
assessment as soon as possible after ventricular drainage. We would aim
for MAP 80-100 and normocarbia pre-coil/clip. Increasingly of late we
have been getting a CT angio with the very first CT ("thunderclap
headache or sudden collapse -- apparent SAH") and sometimes that CTA
alone, along with the CNS findings, has determined the choice of coil or
clip. The latest 3-D software is fantastic. If the patient can obey
commands and there is no mass lesion (even with hemiparesis) we would
get coil or clip at the next available opportunity (usually 12-48 hours
after ICU admission) and not express too much of a preference either way
-- leaving the neuroradiologists and neurosurgeons to sort it out based
on the neuroanatomy and relative risks of each procedure. Currently
there are about 120 patients clipped and ~50 coiled per annum but the
proportion is reversed in the ICU patients -- we only get about half the
SAH patients. Usually we find that it is easier to get an emergency
coiling than clipping and neuroradiologists (and surgeons) are often
very happy with our suggestion -- please angio and proceed straight to
coil immediately if anatomy is suitable. Post coil or clip we aim for
MAP 100-120, continue full dose nimodipine and get a sedative-free CNS
assessment ASAP. We don't use nitrates for the reasons Tom says and we
don't have nicardipine available here. Usuallly hypertension
pre-aneurysm exclusion is adequately controllable with nimodipine 60 mg
4-hourly (as in the BANT trial)and IV then enteral betablocker. A few
patients we give old-fashioned hydrallazine to (after ensuring that they
are betablocked) as we think that this is probably safe from a cerebral
vasodilatory point of view. The very odd patient gets renal failure
(despite MAP etc) with nimodipine and we have shied away from ACE
inhibitors. There is a fair old incidence of post-aspiration nosocomial
chest sepsis too in these patients and we are more comfortable with less
durable agents (than 'prils) in patients at risk of this. We are
currently discussing an early surgery versus early coiling study for
bad-grade patients. My prejudice is that coiling is best for bad grade
patients (except those who also need evacuation of a mass lesion) and
clipping is best for good grade patients. The last neurosurgeon in the
"wait ten days" school of aneurysm surgery here retired a year ago (I
worked for him in my first house officer job in Nov 1974). At the time
that we starting collecting prospective data on ICU patients (1984), we
had a 75% mortality for ventilated bad-grade SAH patients. Waiting ten
days was a disaster -- they usually either rebled, got vasospasm and
infarction or got sepsis before the ten days were up. Now the mortality
is much better (but still ~30% for the bad ICU subset we get now).
Please keep us informed of what happens.
 

ECG changes following SAH occur in 50-100% of cases. Segmental wall motion abnormalities on echocardiography, and mild cardiac enzyme elevations have also been reported after SAH. This condition may be (incorrectly) interpreted as coronary insufficiency. (Patients with SAH have been treated with thrombolysis, and been brought to the cathlab, and received clopidogrel). However, these changes are often reversible and do not respond to administration of coronary vasodilatators. Neurogenic myocardial stunning is a reversible dysfunction of the myocardium with ischemic ECG changes, decreased arterial blood pressure, decreased cardiac output, mild cardiac enzyme elevations (CK, CK-MB, troponin T), and SWMA. Outburst of catecholamines from the sympathetic nerves in the heart may be directly cardiotoxic or may cause cardiac ischemia due to transient coronary vasospasm. Similar things can be seen in phaechromocytoma, cocaine abuse and epinephrine overdose.

Sodium Nitrite 0.2 microM/min/kg will be the solution to vasospasm

Review article of current developments in aneurysmal SAH(Crit Care Med 2006;34(2):511)

Coiling vs. Clipping

ISAT pitted coiling vs. clipping (most pts were an circulation) Outcomes were better in the coiling group, though rate of rebleed @ 1 year was slightly higher

recent data has shown identical midterm mortality

Posterior circ all get coils

Dx of Vasospasm and Impeding Ischemia

MCA blood flow velocities > 200 cm/sec are associated with vasospasm

Small studies are showing CTA is as good as angio for dx vasospasm

EEG may also have a role

hydrocephalus and vasospasm will present in the same way; pt will become less interactive. Vasospasm will eventually go on to cause focal deficits while, hydrocephalus will cause elevated ICPs

Vasospasm may be caused by spreading depression of Leao, macroscopic depression of electrical activity from sustained cellular depolarization

Occurs between 3-14 days (8 days is most common)

middle aged pts at highest risk

Trans-cranial dopplers daily?

Lindegard ratio >3 sens, >6 specific

Nimodipine 60 mg PO q4

starts with decrease in mental status, non-focal delerium

temporarily related to CSW

Management of Vasospasm (delayed cerebral ischemia)

Hemodynamic Augmentation=triple H therapy

hypertension, hypervolemia, hemodilution

SR and MAs showed no benefit to this treatment plan

Triple H Therapy

May be better to go with an inotrope like dobutamine

CO values more important than ABP

SBP>180 (180-220), CI>4, CVP>8, Hb>10

Use of 5% albumin

Intraaortic balloon pump can also be used

Transluminal balloon angioplasty is extremely effective at breaking vasospasm, but only in vessels it can reach

Intra-arterial delivery of vasodilators can also be accomplished

Cerebral Protection

nimodipine's benefit is as a cerebral protectant rather than as a vasodilatory agent

Mag and Statins may also have a role in high grade injuries

Nicardipine

Neurology 1998;50:876

J Neurosurg 1993;78:548

J Neurosurg 1993;78:537

Antithrombotic Therapy

Thrombolytics infused into the subarachnoid space may have benefit

Seizure Prophylaxis

use it any aSAH pt with stroke or focal pathology, but it may cause more problems than it solves.

Cerebral Salt Wasting

renal salt loss leads to hypovolemia and negative sodium balance

0.2 mg of fludrocortisone iv or po bid may prevent intravascular depletion

atrial natriu. peptide up in SAH

Management of Cardiac Dysfunction

pts will have cardiac dysfunction which may result in APE, but neurogenic pulm edema can also exist independently

Neurosurgery. 1982 Mar;10(3):301-7.
Related Articles, Links



Prevention of vasospasm by early operation with removal of subarachnoid blood.

Mizukami M, Kawase T, Usami T, Tazawa T.

Sixty-four patients who were operated on within 4 days after acute subarachnoid hemorrhage are included in this study. All patients underwent preoperative computed tomographic (CT) scanning, and the amount and distribution of subarachnoid blood clot were noted. Operation was carried out by the frontobasal lateral approach, and the subarachnoid clot was removed by microsurgical suction-irrigation after clipping of the aneurysm. Immediate postoperative CT scanning was performed to evaluate the completeness of the subarachnoid blood clot removal. The presence or absence of postoperative vasospasm was determined with angiography performed between the 7th and 10th postoperative days. All patients were, of course, also evaluated for evidence of neurological deterioration. Approximately two-thirds of the patients in this series showed high density subarachnoid blood clot on the preoperative CT scan. The postoperative CT scans showed that it was possible to remove the majority of the blood clot except that located in the frontal interhemispheric fissure, the posterior part of the insular cistern on the approached side, and all of the insular cistern on the contralateral side. There was no spasm or only mild spasm in any site where the blood clot had been successfully removed. Delayed neurological deficits occurred only in those cases in which subarachnoid blood clot remained in the cisterns. These results suggest that it is possible to prevent intracranial arterial spasm and associated neurological deterioration by early operation and removal of clotted blood from the subarachnoid space.

 

Medical Complications:

(Current Opinion in Critical Care 2006;12(2):78)
 

Fever
Fever (defined as a body temperature of >= 38.3°C) is a frequent event in patients with SAH (41–54%, see Fig. 2) [11,12] and in neurocritical care patients in general [13]. In patients with acute brain injury fever leads to augmentation of cerebral edema and intracranial pressure [14,15], exacerbation of ischemic injury [16], significant decrease in arterio-jugular difference in oxygen content (ratio of oxygen consumption to cerebral blood flow) [14], and depression of the level of consciousness [17]. Fever after SAH is significantly associated with an increased risk of symptomatic vasospasm [12] and with poor outcome (moderate-to-severe disability or death) at 3 months [11,12,17] (see Fig. 3). Infection (pneumonia, urinary-tract infection, catheter-related bacteremia, upper-respiratory-tract infection, meningitis) can be identified in approximately 75% of febrile SAH patients [12]. This means that, in the remainder, the cause of fever may be central or neurogenic in etiology. In a study of fever after SAH at Columbia University Medical Center, risk factors included poor admission grade, extent of intracranial blood, cerebral infarction, and pneumonia [17]. Fever is also a common component of the systemic inflammatory response syndrome, which has been shown to predict poor outcome in SAH patients [18].



Fever control can now be achieved by means of core-temperature-controlled surface or endovascular cooling devices. Feasibility studies have demonstrated safe and effective fever control in febrile SAH patients refractory to acetaminophen treatment using the Celsius Control System (Innercool, San Diego, California, USA) [19•], and a single-center randomized trial showed a 75% reduction in fever burden with the Artic Sun Temperature Management System (Medivance, Louisville, Colorado, USA) compared to a regular cooling blanket [20•]. This confirms the results of a previous multicenter fever-control trial comparing a catheter-based heat-exchange system, the CoolGard/CoolLine system (Alsius, Irvine, California, USA) plus standard fever management (utilizing acetaminophen, ibuprofen, and cooling blankets) to standard therapy alone, in which a 64% reduction in fever burden was shown [21].

With all forms of cooling, the main limitation to achieving the set target temperature is insufficient control of shivering which increases the metabolic rate, oxygen consumption, and CO2 production, and may potentially adversely affect cerebral oxygenation and intracranial pressure [19•]. It is the natural mechanism of the human body to conserve heat if the body temperature falls below the hypothalamic set point assessed by the pre-optic region of the hypothalamus. Potentially effective anti-shivering interventions are listed in Table 2. Treatment guidelines almost universally advocate maintenance of normothermia for all febrile patients with SAH, despite little evidence to support this practice in the form of randomized controlled trials. Prospective clinical trials are needed to assess the impact of fever control with systemic surface or intravascular cooling devices on development of vasospasm and outcome after SAH.



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[Email Jumpstart To Image] Table 2 Interventions to relieve shivering during active cooling to achieve normothermia with systemic surface or intravascular cooling devices

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Anemia
Anemia after SAH most likely results from the combined effects of SAH-related reduction in red blood cell mass [22], bed rest, phlebotomy, and hemodilution from fluid administration. In our SAH cohort, anemia (defined as hemoglobin < 9 mg/dl, requiring blood transfusion) occurred in 36% of 580 patients, and was the second most common medical complication in our SAH cohort [11] (Fig. 2). Anemia treated with blood transfusion is associated with an increased risk of mortality and poor functional outcome at 3 months after SAH [11] (Fig. 3) and at 6 months [23]. Administration of blood during the hospital course after aneurysm surgery has also been associated with an increased risk of asymptomatic and symptomatic angiographically confirmed vasospasm [23]. In another study, blood transfusions were significantly related to worse outcome among SAH patients with vasospasm [24].

It is unclear whether anemia after SAH reflects general illness severity, or whether the treatment for anemia – blood transfusion – directly contributes to poor outcome. Transfused red blood cells may be depleted of NO [25], an endogenous vasodilator that affects vasoconstriction of cerebral arteries and arterioles during vasospasm. Thus, transfusion may result in dilution of this active vasodilatory substance, which may subsequently worsen vasospasm or predispose to intraoperative cerebral vasoconstriction [23]. Stored red blood cells have proinflammatory effects and may potentially induce immunodysfunction or neutrophilic and polymorphonuclear cytotoxicity [26], which might add to the inflammatory component of vasospasm [23]. The deformability of transfused erythrocytes is reduced [27], which may lead to microvascular sludging or obstruction, thus provoking ischemia [23]. While red blood cells are stored, ATP and 2,3-diphosphoglycerate are depleted [27], which results in altered oxygen binding or release. This may cause local tissue hypoxia [23]. Transfused erythrocytes enclose iron which could increase oxidative processes in its ferrous form [28] and aggravate ischemia [23]. Storage of red blood cells has been found to generate interleukin-1, -6, and -8 and tumor necrosis factor [alpha] [29] which may augment ischemia and edema formation [23]. Given all the potential detrimental effects of red blood cell transfusion, efforts directed at prevention of anemia after SAH with erythropoietin should be investigated [30], particularly given its potential neuroprotective properties [31].

Hyperglycemia
Hyperglycemia is known to have an adverse effect on outcome in patients with acute ischemic stroke, and increase the likelihood of intracranial hemorrhage after thrombolytic therapy [32–34]. In our SAH population, hyperglycemia exceeding 11.1 mmol/l (200 mg/dl) occurred in 30% (Fig. 2) and was a significant predictor of poor functional outcome and mortality (mRS 4–6) at 3 months after SAH [11] (Fig. 3). When mean daily glucose burden (defined as the excess of the highest measured value above 5.8 mmol/l or 105 mg/dl) was analyzed, hyperglycemia was found to be more strongly associated with disability and loss of high-level functional independence than with mortality at 3 months, suggesting that hyperglycemia may primarily contribute to physical deconditioning [35]. In another study, elevated blood glucose levels on admission in 149 SAH patients were significantly predictive of unfavorable outcome defined as death, vegetative state, or severe disability at 12 months after SAH [6]. A retrospective study of 352 SAH patients at Massachusetts General Hospital identified hyperglycemia (mean inpatient blood glucose value >= 140 mg/dl) in 73% of patients, and found an independent association with symptomatic vasospasm and with poor outcome at discharge (mRS >= 3) [36•]. These findings are in contrast to a different analysis of 175 patients in which elevated admission glucose was not significantly predictive of delayed cerebral ischemia, despite an association with poor outcome at 3 months (death or moderate-to-severe disability) after adjustment for age, clinical and Fisher grade, intraventricular and intracerebral hemorrhage, and permanent artery occlusion during aneurysm surgery [37].

Acute brain injury may lead to a generalized stress response, which may explain the high frequency of hyperglycemia after SAH in patients who do not have a history of diabetes mellitus [38]. In our study, higher Hunt–Hess grade, elevated admission APACHE II physiological subscores, older age, and history of diabetes mellitus were predictive of hyperglycemia [35], demonstrating a relationship between the extent of neurological injury, physiological derangement, and hyperglycemia. Hyperglycemia is most likely just one aspect of global homeostatic derangements after SAH, including systemic inflammatory response syndrome, autonomic nervous system instability, hypothalamic-pituitary axis dysfunction, and neurogenic cardiopulmonary injury [39].

Strict glucose control has been associated with reductions in intracranial pressure, duration of mechanical ventilation, length of stay in the hospital, use of vasopressors, frequency of seizures and diabetes insipidus in critically ill neurological patients [40••], and has been shown to reduce mortality in critically ill surgical patients in the intensive care unit [41]. A small trial of 55 patients with SAH demonstrated feasibility and safety of continuous insulin infusion for glucose values exceeding 7 mmol/l with glucose assessments every 2 h [42]. However, more safety trials of intensive insulin therapy in SAH as well as efficacy studies exploring long-term outcome after SAH are needed.

Cardiac complications
Hypertension (systolic blood pressure > 160 mmHg treated with continuous intravenous medication, 27%) and hypotension (systolic blood pressure < 100 mmHg treated with vasopressors, 18%) are common medical complications after SAH, whereas life-threatening arrhythmia (8%), myocardial ischemia (6%) and successful resuscitation from cardiac arrest (4%) occur rarely (Fig. 2). Electrocardiographic abnormalities are found frequently in SAH patients and encompass ST segment alterations (15–51%), T-wave changes (12–92%), prominent U waves (4–47%), QT prolongation (11–66%), conduction abnormalities (7.5%), sinus bradycardia (16%) and sinus tachycardia (8.5%) [43,44], but do not contribute significantly to morbidity or mortality after SAH [43].

Neurogenic stunned myocardium is the most severe form of cardiac injury after SAH. It is caused by an excessive release of catecholamines from the cardiac sympathetic nerves, and characterized histologically by predominantly subendocardial contraction band necrosis [45]. The clinical syndrome of severe acute stunned myocardium is characterized by transient metabolic acidosis, cardiogenic shock, pulmonary edema, widespread T-wave inversions with a prolonged QT interval, and reversible left-ventricular-wall motion abnormalities as seen by echocardiography [45]. The most important risk factor for neurogenic stunned myocardium is poor clinical grade, although females seem to be relatively over-represented as well [46•].

Minor cardiac enzyme elevations are frequently identified after SAH, but their significance has up until now been unclear. An analysis of 253 SAH patients deemed at risk for myocardial injury revealed admission cardiac troponin I elevation in 68%. Troponin levels peaked at 1.7 days, and left-ventricular-wall motion abnormalities were identified by echocardiography in 22%. Higher Hunt–Hess grade on admission, intraventricular hemorrhage or global cerebral edema on admission computed tomography, loss of consciousness at ictus, more severe admission physiological derangements, and an abnormal admission electrocardiography were predictive of increased cardiac troponin I levels. The association with intracranial pathology underlines a neurogenic mechanism of cardiac injury. Troponin I elevation was associated with a significantly increased risk of abnormal left-ventricular-wall motion abnormalities on echocardiography, pulmonary edema, hypotension requiring vasopressors, delayed cerebral ischemia, and cerebral infarction from any cause. Thus, left-ventricular dysfunction and impaired hemodynamics may impair cerebral blood flow. Troponin I elevation also independently predicted severe disability and death at hospital discharge [47•].

Another prospective study found peak troponin I levels of > 1.0 µg/l in 20% of 223 SAH patients. In this study female gender, larger body surface area, Hunt–Hess grade >= III, higher heart rate, lower systolic blood pressure, higher doses of phenylephrine, higher left-ventricular mass index (increased oxygen demand), and shorter time from SAH symptom onset were independently associated with troponin I elevations within 2 days of symptom onset [46•]. This again emphasizes the impact of the initial severity of brain injury as assessed by Hunt–Hess grade on cardiovascular function, and demonstrates the adverse effects of myocardial injury on cardiac performance. Further research is required to test cardio- and neuroprotective intensive care management strategies which may improve outcome after SAH.

Pulmonary complications
Pulmonary complications did not have an independent impact on neurological outcome at 3 months, but remained common and troubling. The most frequent pulmonary complications included pneumonia (20%), pulmonary edema (14%), pneumothorax (3%), and pulmonary embolism (0.3%; Fig. 2) [11]. However, a previous analysis has linked pulmonary events to an increased frequency of symptomatic vasospasm after SAH, which may reflect fluid overload related to more aggressive hypertensive and hypervolemic therapy [48].

A recent retrospective review suggested that utilization of a pulmonary artery catheter during the vasospasm period in SAH targeting an optimal pulmonary artery wedge pressure (10–14 mmHg) may decrease the incidence of pulmonary edema and sepsis and decrease mortality [49].

Electrolyte abnormalities
Hyponatremia occurs in 30–40% of SAH patients. It may be the result of the syndrome of inappropriate excretion of antidiuretic hormone, cerebral salt wasting, or both. Hypomagnesemia (37%), hypokalemia (27%), and hypernatremia (approximately 20%) are also quite common after SAH [44,50,51]. In our cohort, hyponatremia occurred in only 14% (Fig. 2), which might be explained by the standard administration of isotonic saline solutions and strict avoidance of free water in our management protocol [11]. However, hyponatremia did not have any prognostic significance in our study [11], nor has it in others [51]. The 22% frequency of hypernatremia in our study almost certainly reflects treatment for cerebral edema with mannitol or hypertonic saline solutions, and therefore was mostly iatrogenic. Only 4% of our patients experienced diabetes insipidus [11].

Infections
The most common infections during the hospital course after SAH include pneumonia (20%), urinary-tract infections (13%), bloodstream infections (8%), and bacterial meningitis/ventriculitis (5%; Fig. 2) [11]. None of these infections were independently predictive of poor functional outcome and mortality at 3 months [11]. However, pneumonia and urinary-tract infection were significantly associated with the occurrence of delayed cerebral ischemia. Therefore, hospital-acquired infections should be treated aggressively, and further studies of the associations of infections with neurological complications are necessary.

Other rare complications
Renal failure, hepatic failure, deep-vein thrombosis, and gastrointestinal bleeding occurred at a frequency of less than 5% in our SAH population and had no impact on neurological outcome (Fig. 2) [11]. A study of 100 SAH patients found a low ratio between the lowest platelet during the hospitalization and the admission platelet count (< 0.7) to be an independent predictor of symptomatic vasospasm [52]. This may be explained by increased platelet aggregation and substance release from the platelets, resulting in microcirculatory dysfunction [52]. The role of platelet dysfunction in the pathophysiology of vasospasm requires additional studies.

Terson's Syndrome

the real reason to examine the fundi is Terson's syndrome, the development of subhyaloid hemorrhage in the setting of SAH.  This requires the intervention of the ophthalmologist, often a vitrectomy, to prevent retinal detachment, as well as to remove the clot obstructing vision.

(Bleck, Tom)

CT Angiogram

scary missed aneurysms by LP

TABLE 1. Characteristics of Patients with Positive CTA Findings

CT = computed tomography; LP = lumbar puncture; CTA = computed tomographic angiography; MCA = middle cerebral artery; SAH = subarachnoid hemorrhage; ACOM = anterior communicating artery.

Adverse events attributable to negligence have been found to be significantly lower in teaching hospitals,²⁴ although the reasons for this are generally not well understood. Before these differences can be addressed, other explanatory factors at the hospital and physician level need to be explored. Whereas clinical judgment is likely to play an important role in the accurate diagnosis of SAH in the ED,²⁶ standardization of the diagnostic approach to potential SAH patients may not fully address the problem. Current efforts to derive a clinical decision rule to rule out SAH in headache patients have been carried out among patients attending teaching hospital sites,^32,33 and the effectiveness of rules could be limited if their implementation or interpretation varies between community and teaching hospitals.

We found that the crude mortality rate was lower among patients with a missed SAH, but this analysis should be interpreted with caution because we were unable to control for differences in SAH severity, and cannot account for patients who were misdiagnosed but subsequently died at home without being admitted for SAH. Our results are similar to another study which found the crude mortality rate to be lower among misdiagnosed patients, but higher once SAH severity was accounted for.¹⁰ Although triage levels among missed SAH patients in our study worsened between the prior and subsequent ED visit, they were still less acutely ill on their admitting visit than those diagnosed at their initial ED visit. Rebleeding, the most serious complication,³¹ typically occurs within days of an initial SAH,^34,35 but there may have been less time for this and other SAH-related complications to develop compared with other studies because the majority returned within a few days.

We identified SAH patients retrospectively through administrative health databases; therefore, our data provided limited detail regarding clinical characteristics. Despite the limitations of this data, SAH has been found to be coded with a reasonably high degree of accuracy in validation studies of hospital discharge data.^36,37 At the same time, it was not feasible to derive population-based rates of missed SAH using a more detailed collection method, such as chart review, or to undertake a prospective study at such a large number of hospitals over so many years. This method has been previously used to identify misdiagnoses using administrative data¹⁷; however, our definition of prior related visits for SAH patients has not been validated, which could lead to some misclassification. Previous studies have used a variety of methods and definitions to identify missed SAH, given the absence of a standard method to identify misdiagnoses, and none have been externally validated. Any misclassification should not affect our analysis of predictors of missed SAH so long as it is nondifferential. Although we were only able to include Ontario residents with valid health cards, out-of-province patients comprised <1% of the original study population, and we expect the number of persons without a health card in a publicly funded universal healthcare insurance system to be small. We could not ascertain prior related visits among missed SAH patients who attended the ED but died without re-admission. Hence, both the numbers of missed SAH and the associated mortality rates herein may be underestimated. In addition, we defined the prior related ED visits according to conditions described as misdiagnosed SAH.^10,11,15,18 It is possible that some of these earlier diagnoses were not related to the subsequent presentation with SAH, but the narrow time frame of 14 days makes this less likely to be so. We extended the time period for misdiagnosis to 28 days and the rate remained virtually unchanged, similar to another study that found that the delay to SAH diagnosis among ED patients did not exceed 19 days (Mayer SA, unpublished data, 2004). Moreover, we have no reason to believe this would systematically occur more often in nonteaching than in teaching hospitals, and any misclassification would bias the results toward a null finding. The mechanisms that led patients to return to hospital after misdiagnosis were also unknown; they may have returned for lack of improvement of symptoms, worsening clinical condition, or may have been called back given abnormal results. In any case, however, the repeat visits would be captured in our databases and would still be appropriately identified as a missed SAH. Finally, we were unable to obtain data regarding other factors that may have explained the high rates of missed SAH in nonteaching hospitals, such as availability or routine use of CT angiography, MRI/angiography or neuroradiology consultants at each ED. These and other potential explanatory mechanisms require further study.

Our findings suggest that rates of missed SAH varied considerably across individual EDs, regardless of hospital type, but overall are lower than previously reported. Administrative data could be a valuable tool for identifying differences in misdiagnosis rates, as has been done previously for complications,^38,39 targeting interventions to reduce these rates, and monitoring the impact of interventions.

Summary
About 1 in 20 persons with SAH are missed on their first presentation to an ED, and the risk is greater in patients with low acuity presentations. The risk is also greater in nonteaching hospitals, but this could not be attributed to annual ED SAH volume or CT availability. Other contextual factors, such as physician training and experience, availability of consultants and other resources such as diagnostic technologies, or differences in diagnostic protocols will need to be evaluated before effective interventions to reduce missed SAH rates can be developed.

Acknowledgments

This study was supported by a grant from the Peter Lougheed Medical Research Foundation. Dr Schull has a Career Award from The Canadian Institutes of Health Research.

Disclosures

None.

Footnotes

Received September 8, 2006; revision received October 16, 2006; accepted November 15, 2006.

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J Neurosurg. 2000 Jun;92(6):971-5.


Adverse effects of limited hypotensive anesthesia on the outcome of patients with subarachnoid hemorrhage.

Chang HS, Hongo K, Nakagawa H.

Department of Neurological Surgery, Aichi Medical University, Japan. chang@aichi-med-u.ac.jp

OBJECT: This study was aimed at clarifying the effect of intraoperative hypotensive anesthesia on the outcome of early surgery in patients with subarachnoid hemorrhage (SAH) caused by saccular cerebral aneurysms. Other factors were also screened for possible effects on the outcome. METHODS: Hospital charts in 84 consecutive patients with SAH who underwent aneurysm clipping by Day 4 were examined. Possible factors affecting the outcome were analyzed using multiple logistic regression with the dichotomous Glasgow Outcome Scale score as the outcome variable. The relationship between the intraoperative hypotension and the occurrence and severity of vasospasm was studied using both single- and multivariate analyses. CONCLUSIONS: Intraoperative hypotension had a significantly adverse effect on the outcome of SAH. Hypotension was also related to more frequent and severe manifestations of vasospasm. A long-lasting effect of brain retraction is possibly the cause of this phenomenon. The data contained in this study preclude the use of intraoperative hypotension even in a limited form.

Neurocritical Care