Lower BP by ~15%
with PRN IV hydralazine,labetalol, nicardipine
Lower BP cautiously, only as needed to decrease end-organ damage, prevent abrupt drops.
Avoid nitrates.
>130
<130
Risk of end-organ damage?
EKG changes, elevated troponins, proteinuria, high creatinine, heart failure/
pulmonary edema, aneurysmal dissection, etc.
Yes No
No treatment MAP = [SBP + 2 × DBP]/3
MAP, mean arterial pressure; SBP, systolic blood pressure; DBP, diastolic blood pressure; EKG, electrocardiogram; PRN, as needed; IV, intravenous; BP, blood pressure.
T R E A T M E N T O F C E R E B R A L E D E M A
Cerebral edema in ICH can occur as a result of the direct effects of hematoma volume and edema, as well as hydrocephalus due to intraventricular hemorrhage (IVH) or ventricular compression. In patients with a decreased level of conscious- ness (Glasgow Comma Scale score≤8), clinical evidence of cerebral herniation, or those with significant IVH or hydrocephalus, ICP monitoring with a ventricular or parenchymal catheter should be considered. (See ICP treatment Algorithm 60.1 in Chapter 60.)
S E I Z U R E S
The primary neuronal damage and blood products increase seizure risk after ICH.
Seizures occur in 5% to 15% of these patients, usually in the first few days of hospital- ization. Prophylactic anticonvulsant therapy is not indicated in ICH, but in patients with depressed mental status out of proportion to the degree of brain injury, contin- uous electroencephalography should be considered. Patients with clinical seizures and patients with mental status changes and electrographic seizures should be treated with anticonvulsant therapy.
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TABLE 54.3 Indications for Neurosurgical Intervention After Intracerebral Hemorrhage
rPosterior fossa or temporal lobe hemorrhage>3 cm rICH causing hydrocephalus or brainstem compression rHydrocephalus or IVH requiring EVD
rComplicated cases requiring ICP monitoring
ICH, intracerebral hemorrhage; EVD, external ventricular drain; IVH, intraventricular hemorrhage;
ICP, intracranial pressure.
N E U R O S U R G I C A L I N T E R V E N T I O N
In patients with a cerebellar hemorrhage who are deteriorating neurologically or who have brainstem compression and/or hydrocephalus from ventricular obstruction, surgi- cal removal of the hemorrhage is recommended as soon as possible (Table 54.3). In most other cases of ICH, the utility of surgical evacuation remains controversial. For patients with supratentorial lobar hemorrhage>30 mL and within 1 cm of the surface, evacu- ation by standard craniotomy may be considered, although strong evidence is lacking.
G E N E R A L C A R E
Patients with ICH, like all critically ill patients, are at risk for numerous complica- tions including myocardial infarctions, heart failure with pulmonary edema, deep vein thrombosis (DVT), aspiration pneumonia, urinary tract infections, pressure ulcers, and orthopedic complications (contractures etc.). Sequential compression devices in addition to elastic stockings should be used from admission, and subcutaneous low- molecular-weight heparin or unfractionated heparin for DVT prophylaxis can be started after 48 hours if there is no evidence of hematoma expansion. Spontaneous lobar ICH in particular carries a relatively high risk of recurrence, thus avoidance of long-term anticoagulation for nonvalvular atrial fibrillation in these patients is rec- ommended. In the presence of a clear indication for anticoagulation (e.g., mechanical heart valve) or antiplatelet therapy (e.g., coronary artery stents), it is reasonable to restart anticoagulation in nonlobar ICH in 2 to 4 weeks and antiplatelet therapy in all ICH 1 to 2 weeks after documentation of cessation of bleeding.
S U G G E S T E D R E A D I N G
American Heart Association Stroke Council and Council on Cardiovascular Nursing. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association.Stroke.
2010;41;2108–2129.
55 ComaMichael A. Rubin
Coma is a state of persistent unresponsiveness. It can occur because of a primary neurologic disorder or as a complication of a systemic pathology. Either way, there must be a disruption of the normal function of either the reticular activating system in the brainstem or both cerebral hemispheres. The underlying cause of coma may be immediately apparent on the basis of the initial history and examination; however, in other situations, it may take days to discern the cause of the severe encephalopathy.
Although coma is an extremely serious situation, an extensive evaluation may result in finding the cause and providing the treatment of coma recovery.
E V A L U A T I O N A N D M A N A G E M E N T O F C O M A
Although the depressed mental states along the spectrum that leads to coma have been described by terms such asstupor, lethargy, andobtundation, the terms are used differently by various sources and are usually not specific enough. When following a patient’s response to therapy, a more detailed description is valuable and has higher interrater reliability. The amount of stimulation required to elicit a response and what the response is should be identified. The Glasgow Coma Scale is widely used as a standard method to describe neurologic function in a quick and concise manner (Table 55.1), and it carries prognostic value for patients with traumatic brain injury.
Initial Evaluation and Stabilization
Concurrent with the investigation of the cause of coma, appropriate resuscitative measures should be provided. Intubation is usually necessary for airway protection;
fluids and/or vasopressors are instituted for hypotension; warming blankets may be required for hypothermia. Laboratory tests including a rapid blood glucose test, arte- rial blood gases, electrolyte panel, chemistries, blood counts, cultures, toxin screens, and thyroid and liver function tests should be ordered. In addition, brain imaging is important to evaluate for a surgical cause of coma. Other tests such as lumbar punc- ture and electroencephalography may be useful depending on the presentation. The initial examination during stabilization should guide the priorities of the work up. For example, pupillary abnormalities suggest an underlying intracranial structural lesion with elevated intracranial pressure requiring expedient head computed tomography and neurosurgery consultation. The presence of fever, nuchal rigidity, or skin rash should prompt lumbar puncture and antimicrobial therapy.
Many emergency departments employ a “coma cocktail,” including intravenous administration of thiamine, glucose, and naloxone. Thiamine protects against the potentially fatal Wernicke encephalopathy and should be given to all patients with
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TABLE 55.1 Glasgow Coma Scale Best eye opening
Spontaneous 4
With voice only 3
With pain only 2
None at all 1
Best verbal response
Coherent speech 5
Confused intelligible speech 4
Inappropriate words 3
Incomprehensible sounds 2
No verbal output 1
Best motor response
Follows commands 6
Localizes pain stimulia 5
Withdraws to pain stimuli 4
Decorticate posturing 3
Decerebrate posturing 2
No movements at all 1
aLocalizing pain stimuli refers to gaze deviation, head turning, or hand movements toward the stimulus.
unexplained coma or suspicion of long-term alcohol abuse and/or malnutrition. Glu- cose is withheld until hypoglycemia is confirmed and thiamine has been given. Nalox- one is useful as a therapeutic agent in the reversal of opioid toxicity, whereas flumazenil is equally effective in a benzodiazepine overdose. Caution should be exercised as rapid reversal in long-term users could precipitate seizure.
General and Neurologic Examination
After the initial assessment and stabilization of the patient, a more thorough evalua- tion may proceed. History of present and recent illness should be discussed with the caregivers or relatives. Much can be learned from clinical records from outside facilities as to the time course involved in the progression of the disease and any precipitating events. The cause may be apparent from the history; in some cases, the general phys- ical examination may reveal signs of underlying diseases (such as rashes, liver failure stigmata, murmurs, etc).
The neurologic examination is focused on evaluating the function of the struc- tures previously mentioned (brain stem and bilateral hemispheres) whose dysfunction is responsible for coma. This includes level of alertness and awareness, cranial nerve reflexes, motor function, and respiratory pattern. Consciousness is assessed by record- ing response to increasing intensities of stimuli. One begins with the name softly, then loudly, then with a gentle shake. If these fail to arouse the patient, a painful stimulus (supraorbital pressure, sternal rub, or temporomandibular pressure) should be applied.
Also note if the stimulation must be repeatedly applied to maintain alertness or if the patient stays awake once aroused. If family is present, be sure to inform them the purpose of your examination, especially if painful stimuli are being applied.
Neurologic Disorders rComa 4 4 7