Bongard Frederic , Darryl Sue. Diagnosis and Treatment Critical Care

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NEUROSURGICAL CRITICAL CARE

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and vomiting, photophobia, nuchal rigidity, depressed level

of consciousness (eg, somnolence, obtundation, or coma),

cranial nerve palsies, and motor abnormalities can occur.

The severity of symptoms is related to the site and extent of

the bleeding. Following aneurysmal subarachnoid hemor-

rhage, the patient is categorized by grade using the Hunt and

Hess classification system (Table 31–3). This system has been

widely accepted and is the equivalent of the Glasgow Coma

Score in trauma patients.

B. Imaging Studies—

1. CT scanning—Ninety percent of patients with subarach-

noid hemorrhage have evidence of subarachnoid blood on

initial CT scans obtained within the first 48 hours after rup-

ture. Scanning also detects intraparenchymal and intraven-

tricular bleeding. The extent and location of subarachnoid

hemorrhage can help to determine the location of the

aneurysm and identify patients at highest risk for developing

cerebral vasospasm. Rebleeding, hydrocephalus, and cerebral

infarction also can be verified using this technique.

2. Angiography—Once the diagnosis of subarachnoid hem-

orrhage has been established, a form of cerebral angiography

should be performed unless a surgical lesion such as a signif-

icant intraparenchymal hematoma is present and requires

emergent lifesaving evacuation. Angiography is required

prior to aneurysm surgery to localize the aneurysm, define its

anatomy, and identify areas of cerebral vasospasm that may

require postponement of surgery. All cerebral vessels should

be imaged because of the occurrence of multiple aneurysms

in 15–20% of patients.

3. Transcranial Doppler ultrasonography—Transcranial

Doppler ultrasonography has become a useful technique for

monitoring patients at risk for developing vasospasm. With

progressive arterial narrowing, blood flow velocity increases

through the constricted segment and can be detected by this

procedure. Since this technique is noninvasive and portable,

it can be performed at the bedside in the ICU. It can detect

arterial narrowing prior to the development of ischemic

symptoms so that therapy aimed at improving cerebral blood

flow can be instituted.

C. Lumbar Puncture—In patients in whom no subarachnoid

hemorrhage is present on CT and the history is suggestive of

rupture of an intracranial aneurysm, lumbar puncture should

be performed. Bloody or xanthochromic fluid is the most

sensitive indicator of subarachnoid hemorrhage. CSF cultures

must be sent to rule out meningitis. However, lumbar punc-

ture never should be performed prior to CT scanning because

patients with elevated ICP are at risk for herniation following

removal of fluid from the spinal subarachnoid space.

D. Laboratory Findings—Coagulation parameters, includ-

ing a platelet count, bleeding time, and prothrombin and

partial thromboplastin times, should be obtained. If abnor-

mal clotting parameters are present, they should be corrected

rapidly because of the increased risk of rebleeding.

E. Electrocardiography—The ECG is abnormal in many

cases of subarachnoid hemorrhage and may identify cardiac

arrhythmias or ischemia that may require treatment.

Treatment

A. Surgery or Embolization—Most centers advocate early

intervention (within 24 hours of rupture) with either surgery

or embolization. Early treatment of the aneurysm has the

advantage of preventing rebleeding and allowing aggressive

therapy for vasospasm should it develop. Because of the risk

of exacerbating ischemia by brain retraction, surgery may be

delayed in patients who are medically unstable or who have

severe vasospasm.

B. Preoperative ICU Therapy—Prior to surgery, treatment

is aimed at reducing the risk of rebleeding and preventing

ischemic complications related to vasospasm. Patients

should remain at bed rest in a quiet setting. Mild analgesics

(not aspirin because of its antiplatelet properties) are used if

headache or neck pain is severe. Stool softeners are useful to

prevent straining, which can increase ICP and promote

rerupture.

C. Blood Pressure Control—Systolic blood pressure should

be maintained below 150 mm Hg; however, hypotension

must be avoided so that cerebral perfusion pressure is not

reduced to ischemic levels. Intravenous administration of

sodium nitroprusside has the advantage of being rapidly

reversible. Mild intravascular fluid augmentation using intra-

venous colloid infusion (5% albumin, 250 mL every 6–8

hours) helps to maintain adequate cerebral perfusion.

D. Reduction of Ischemic Deficits Owing to Vasospasm—

Vasospasm is the most frequent cause of morbidity and mor-

tality in patients admitted after subarachnoid hemorrhage

and occurs in 22–44% of patients. Arterial narrowing may

lead to diminished perfusion and cause infarction.

Vasospasm is induced by products of erythrocyte break-

down, and the risk of developing this complication is related

Grade 1 Asymptomatic, or minimal headache and slight nuchal

rigidity.

Grade 2 Moderate to severe headache, nuchal rigidity, no

neurologic deficit other than a cranial nerve palsy.

Grade 3 Drowsiness, confusion, or mild focal deficit.

Grade 4 Stupor, moderate to severe hemiparesis, early decere-

brate rigidity, and vegetative disturbances.

Grade 5 Deep coma, decerebrate rigidity, moribund rigidity.

Table 31–3. Hunt and Hess grades for the assessment

of patients with subarachnoid hemorrhage.

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688

to the quantity of blood in the subarachnoid space. There is

a peak incidence 4–12 days after subarachnoid hemorrhage,

and vasospasm then resolves gradually. Prophylactic therapy

using calcium channel blockers and mild volume expansion

are only partially effective. Once vasospasm has been diag-

nosed by transcranial Doppler ultrasonography or angiogra-

phy, more intense therapy is warranted. If ischemic

neurologic symptoms are evident, aggressive treatment

should be instituted immediately.

Induced hypervolemia, hemodilution, and hypertension

(triple-H therapy) may augment cerebral blood flow and

prevent ischemic cellular damage. Because cerebral autoreg-

ulation can be impaired after subarachnoid hemorrhage,

hypertension and hypervolemia may increase cerebral blood

flow directly. Decreased blood viscosity by induced hemodi-

lution can improve cerebral blood flow in regions of hypop-

erfusion. The optimal hematocrit is between 31% and 33%.

Oxygen-carrying capacity of the blood is not significantly

reduced in this range. Since aggressive therapy is often

required, placement of an indwelling pulmonary artery

catheter is recommended to monitor hemodynamics.

Therapy should be titrated to ameliorate ischemic symp-

toms. In addition, cerebral blood flow measurements may

aid in documenting adequate perfusion following treatment.

A poor outcome may occur despite triple-H therapy in most

patients with a low Glasgow Coma Score and evidence of

hydrocephalus at the onset of vasospasm.

Oral administration of the calcium channel antagonist

nimodipine (60 mg orally every 4 hours for 21 days) has been

shown to reduce ischemic neurologic deficits attributable to

vasospasm following aneurysmal subarachnoid hemorrhage.

E. Prevention of Seizures—Patients who have sustained

aneurysmal subarachnoid hemorrhage are at risk for seizures

and should receive anticonvulsants (eg, phenytoin, 18 mg/kg

intravenously initially, followed by 300–400 mg daily)

because of the risk of seizure-induced arterial hypertension,

ICP alterations, and local increased cerebral blood flow

requirements.

F. Respiratory Management—Intubation and mechanical

ventilation are required in comatose patients and those with

respiratory compromise. Mild hyperventilation can be useful

to control elevations of ICP.

G. Correction of Electrolyte Disturbances—Hyponatremia

is common following subarachnoid hemorrhage and can

lead to harmful cellular volume changes in the CNS. (Please

refer to the preceding discussion of cerebral salt wasting.)

Correction of hyponatremia should be accomplished care-

fully so that abrupt sodium changes do not occur.

Administration of hypertonic saline (3%) is often necessary

to improve the sodium level and volume depletion.

H. Intracranial Pressure Monitoring—Placement of a ven-

tricular catheter is necessary to monitor ICP in comatose

patients and to treat hydrocephalus if present. This also helps

clear erythrocyte breakdown products, which are associated

with the development of hydrocephalus. Care should be taken

to avoid rapid overdrainage of CSF because abrupt reduction

in ICP may induce aneurysm rebleeding. Many patients even-

tually will require a permanent ventriculoperitoneal shunt.

I. Antifibrinolytic Therapy—Agents such as aminocaproic

acid that inhibit dissolution of the fibrin clot have been shown

to reduce the incidence of rebleeding. However, this positive

effect is offset by an increased risk of permanent ischemic

sequelae and systemic venous thrombosis. Treatment with

antifibrinolytic agents does not improve clinical outcome fol-

lowing aneurysmal hemorrhage and should not be used.

J. Angioplasty—Even though treatment using hypervolemic

hemodilution and induced arterial hypertension is effective,

a significant number of patients do not respond to these

techniques. Balloon dilation angioplasty can mechanically

increase vessel diameter and has been shown to improve

cerebral blood flow and relieve symptoms dramatically.

Cerebral angioplasty is a new technique and is indicated,

where available, in subjects who do not respond to medical

therapy. Intraoperative vasodilating agents such as papaver-

ine also can be infused during catheter angiography.

Adams HP et al: Predicting cerebral ischemia after aneurysmal

subarachnoid hemorrhage: Influences of clinical condition, CT

results, and antifibrinolytic therapy. A report of the Cooperative

Aneurysm Study. Neurology 1987;37:1586–90.

Barker FG, Heros RC: Clinical aspects of vasospasm. Neurosurg

Clin North Am 1990;1:277–88.

Kassell NF et al: Treatment of ischemic deficits from vasospasm

with intravascular volume expansion and induced arterial

hypertension. Neurosurgery 1982;11:337–43.

Newell DW et al: Angioplasty for the treatment of symptomatic

vasospasm following subarachnoid hemorrhage. Neurosurgery

1989;71:654–60.

Ojemann RG, Heros RC, Crowell RM: Surgical Management of

Cerebrovascular Disease. Baltimore: Williams & Wilkins, 1988.

Qureshi AI et al: Early predictors of outcome in patients receiving

hypervolemic and hypertensive therapy for symptomatic

vasospasm after subarachnoid hemorrhage. Crit Care Med

2000;28:824–34. [PMID: 10752836]



Tumors of the Central Nervous System

ESSENTIALS OF DIAGNOSIS



Generalized signs of mass effect.



Aphasia.



Memory disturbance.



Hemiparesis.



Sensory impairment.



Seizure may be the presenting sign.

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689

General Considerations

The critical care of patients harboring brain tumors requires

an understanding of intracranial mass effect, cerebral edema

and the blood-brain barrier, progression of neurologic

symptoms, seizures, and serum electrolyte abnormalities.

Careful serial neurologic examination and physiologic mon-

itoring can result in optimal care for the patient with a brain

tumor.

The signs of either a primary or metastatic brain tumor

are the result of the tumor’s location, mass effect, and rate of

growth and of metabolic disturbances. The Monro-Kellie

doctrine describes the relationship between intracranial vol-

ume (composed of brain, CSF, and blood) and ICP. The brain

can accommodate enlarging mass lesions until a critical vol-

ume is reached. The actual volume tolerated is increased if

growth is gradual. At this point, the ICP increases dramati-

cally (Figure 31–2). Normally, the endothelial tight junctions

of cerebral vessels (blood-brain barrier) prevent the leakage

of large solutes and water into the brain. Vessels in cerebral

tumors tend to have less constant tight junctions and may

lack certain enzymes that degrade vasoactive substances in

the brain such as leukotrienes. Reactive edema fluid thus

accumulates in the extracellular space adjacent to the tumor.

Edema can cause neurologic deterioration by increasing ICP

and causing a midline shift of brain structures. Hyponatremia

can occur in patients with CNS neoplasms and may cause

cytotoxic edema and seizures. This can occur secondary to

cerebral salt wasting, as described earlier. Conversely, hyper-

natremia can result from hypothalamic dysfunction and lack

of antidiuretic hormone response and is referred to as dia-

betes insipidus. These patients lose excessive amounts of free

water. Any serum sodium abnormality can result in altered

mental status and eventually coma and neuronal cell death.

Clinical Features

A. Symptoms and Signs—In contrast to the generalized

symptoms of mass effect, edema, and sodium imbalance,

which include headache, nausea and vomiting, and mental

status changes, the precise location of a tumor can cause spe-

cific neurologic deficits. These deficits include aphasia, mem-

ory or personality disturbances, hemiparesis, and visual or

sensory impairment. In many patients, no neurologic deficit

is present on initial presentation, and a seizure is the first

indication of a CNS neoplasm. In the awake patient, the his-

tory should be taken carefully to determine the exact initial

symptoms and the rate at which the problems have

advanced. This information can indicate the approximate

location in the nervous system and serves as a clue to the rate

of tumor growth. Neurologic examination in the ICU should

include ophthalmoscopy for papilledema, detailed mental

status and language assessment, cranial nerve tests, motor,

sensory, and reflex tests, and testing of cerebellar function.

B. Imaging Studies—A chest x-ray should be performed to

evaluate whether a metastatic source of CNS disease is likely.

The study of choice for a suspected CNS mass lesion is CT

scan or MRI. The latter technique gives finer detail and sub-

tracts the image of cortical bone. It is particularly helpful in

evaluating the posterior fossa and skull base. SPECT-

thallium scans are useful in differentiating high-grade versus

low-grade gliomas.

C. Electroencephalography—Electroencephalography can

localize dysfunctional cortex and epileptogenic foci related to

neoplastic growths.

Differential Diagnosis

Several disease processes should be considered when evaluat-

ing a patient who presents with confusion, headache, dys-

phasia, motor or sensory deficits, seizures, hyponatremia, or

any combination of these findings. Stroke usually presents

with a sudden onset of fixed neurologic signs and differs

from the progressive course of a CNS neoplasm. The gradual

progression of a neurodegenerative disease can result in

symptoms similar to those caused by a mass lesion, but pre-

liminary CT scanning or MRI can rule out this lesion.

Infections such as meningitis, encephalitis, and especially

cerebral abscess can result in global or focal neurologic dys-

function and seizures but frequently are accompanied by

fever, leukocytosis, and (in the case of cerebral abscess) char-

acteristic findings on CT scan or MRI. An important distinc-

tion to be made is whether the mass represents a primary or

metastatic lesion. In the latter, a general physical examination

with radiologic studies and metastatic evaluation is required.

Treatment

A. Immediate ICU Intervention—Treatment of the patient

with altered mental status and findings of papilledema

should begin with protection of the airway and elevation of

the head. The neck should not be flexed nor the head turned

so that optimal venous drainage of the brain via the jugular

veins can be ensured. Hyperventilation, systemic arterial

hypertension, and bradycardia are signs of Cushing’s

response (to raised ICP) and identify a patient in great dan-

ger. Mannitol, 1 g/kg, should be infused rapidly via an intra-

venous catheter. This can be followed by 0.25–0.5 g/kg

every 4 hours accompanied by frequent testing of serum

osmolarity. If seizure activity has been observed or is sus-

pected, a loading dose of phenytoin (18 mg/kg) should be

infused intravenously at a rate not to exceed 50 mg/min. A

daily dose of 300–400 mg can be started the next day. An

immediate CT scan or MRI scan should be obtained. If a

tumor is diagnosed and significant mass effect is present,

placement of a ventricular catheter can be considered in

patients at risk of critical elevation in ICP. Ventricular

catheters allow continuous ICP monitoring and drainage of

CSF. If a neurologic deficit or significant cerebral edema is

present, dexamethasone should be administered. The initial

dose can be as high as 20–24 mg intravenously, followed by

10 mg every 6 hours. This steroid can stabilize endothelial

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690

cell membranes and reduce the accumulation of cerebral

edema. For the severely ill or deteriorating patient, endotra-

cheal intubation should be performed with hyperventilation

to achieve a Pa

of 30–35 mm Hg. Lowering the Pa

con-

stricts cerebral arterioles and reduces the volume of blood in

the brain, thereby alleviating one component of intracranial

volume and increased ICP.

B. Nonoperative Therapy—For patients in poor medical

condition, with multiple metastatic lesions, or with a solitary

tumor in an inaccessible location, stereotactic or CT-guided

biopsy followed by radiation or chemotherapy (or both)

should be instituted. Patients should be weaned from venti-

lator support and ventricular drainage whenever possible.

This may be difficult in a deteriorating patient because of

ethical and family considerations.

C. Surgery—The goals of surgery are to obtain a tissue diag-

nosis and decrease the mass effect by safely removing as

much of the lesion as possible. Craniotomy (removal of a

replaceable bone flap) or craniectomy (removal of sections of

the base of the skull that are not replaced) with microscope-

assisted removal of the tumor can be accomplished with very

satisfactory morbidity and mortality results. Bipolar coagu-

lation forceps, suction and irrigation, ultrasonic aspirators,

and (less frequently) lasers can be used to precisely remove

tumor while limiting damage to surrounding brain. For

tumors in the sellar region, a transnasal, transsphenoidal

approach is most useful. The risks of operation include

increased neurologic deficit, bleeding, deep vein thrombosis,

pulmonary embolism, and death. Mortality rates in most

large centers for patients undergoing removal of intracranial

tumors are under 5%.

Current Controversies and Unresolved Issues

Several aspects of the care of critically ill patients harboring

brain tumors remain controversial. It is still unclear what the

roles of surgery and radiation are in the patient with a low-

grade primary brain tumor. The risk of slow progression of

tumor growth over many years may not outweigh the ill

effects of operation or postirradiation angiopathy and neu-

ronal death (ie, radiation necrosis). Another debatable aspect

of care is the role of chemotherapy for high-grade primary

tumors. Prolongation of survival of 3–6 months with

chemotherapy (beyond the 6–12-month survival of surgery

and radiation alone) may not outweigh the short-term mor-

bidity associated with intravenous antineoplastic therapy.

Deep vein thrombosis and pulmonary embolism repre-

sent a considerable risk to the patient with a brain tumor

who is less mobile or bedridden, yet the role of perioperative

anticoagulation remains an unresolved issue. The duration

of prophylactic anticonvulsant therapy following craniotomy

remains debatable. The range in practice is between 1 month

and 12 months.

Future issues that are likely to make a major impact on the

therapy for critically ill patients with brain tumors include

advances in stereotactic radiation, manipulation of the

blood-brain barrier for selective delivery of antineoplastic

agents to the tumor, and molecular engineering to selectively

transfect tumor cells with gene fragments capable of inducing

differentiation and stopping cellular proliferation. At the pres-

ent time, however, surgical reduction of the total malignant

cell mass and radiation remain standard therapy for malignant

brain tumors. Frameless image-guided neurosurgery has

improved intraoperative visualization of these tumors and

provides hope for improved outcomes in the future.

Brennan RW: Differential diagnosis of altered states of conscious-

ness. In Youmans JR (ed), Neurological Surgery: A

Comprehensive Reference Guide to the Diagnosis and

Management of Neurosurgical Problems, Vol. 1. Philadelphia:

Saunders, 1990.

Plum F, Posner JB: The Diagnosis of Stupor and Coma, 3d ed. San

Francisco: Davis, 1985.

Wilkinson HK: Intracranial pressure. In Youmans JR (ed),

Neurological Surgery: A Comprehensive Reference Guide to the

Diagnosis and Management of Neurosurgical Problems, Vol. 2.

Philadelphia: Saunders, 1990.



Cervical Spinal Cord Injuries

ESSENTIALS OF DIAGNOSIS



Neck pain.



Motor or sensory deficits.



Hypoventilation.



Neurogenic shock.



Priapism.

General Considerations

Approximately 10,000 new cervical and thoracic spinal cord

injuries occur each year in the United States. Most result

from motor vehicle accidents, falls, gunshot wounds, and

sporting accidents. Improved acute management has permit-

ted many patients to survive the initial injury and to have a

near-normal life expectancy. Adolescents and young adults

suffer the highest incidence of spinal cord injuries, with the

majority occurring in young males. Although the loss of

motor and sensory function imposes a catastrophic physical

and emotional handicap, many spinal cord injury patients

are able to return to a nondependent functional state.

Most spinal cord injuries occur in the mobile cervical

region. The cervical cord contains lower motor neurons as

well as long tracts conveying motor and sensory fibers that, if

damaged, can result in variable neurologic dysfunction. In

addition, the cervical cord also conducts vital respiratory and

sympathetic functions that can be damaged following

trauma, leading to devastating respiratory or circulatory

collapse. Secondary events such as hypotension, hypoxia, and

reinjury of the cord can cause further neurologic deterioration.

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691

Because of these unique features, all patients with cervical

cord injuries should be admitted to an ICU staffed by per-

sonnel experienced with the complex care of spinal cord

injuries.

Pathophysiology

There are a number of anatomic, chemical, and vascular

changes that occur in response to blunt injury of the spinal

cord. From immediately following and up to 3–5 hours after

injury, there is focal swelling of the cord owing to disruption

of blood vessels and their endothelial tight junctions. This

leads to localized bleeding and leakage of albumin, neuro-

transmitters, extracellular calcium, lactate, and prostaglandins.

There is a decrease in local blood flow beginning in the cen-

tral regions of the cord and spreading to the surrounding

white matter (centripetal decrease in blood flow). This leads

to worsening edema over the first 2–3 days and central cavi-

tary necrosis over the ensuing week. The level of injury may

rise as much as two vertebral levels in response to these sec-

ondary events. Diminished swelling followed by cord atro-

phy becomes evident after the first week after injury.

Experimental and clinical treatment strategies are aimed at

blocking this cascade of secondary events following spinal

cord contusion. Calcium channel blockers, diuretics, corti-

costeroids, and other free-radical scavengers may be helpful,

although their true efficacy is debated.

Clinical Features

A. History—The key to the initial diagnosis of cervical spine

injury is maintaining a high level of suspicion for an under-

lying bony or ligamentous injury. This is especially true in

patients involved in motor vehicle accidents or significant

falls, particularly if they have other associated injuries such as

head trauma or extremity fractures.

Many trauma patients are conscious and may complain

of neck pain, numbness, or weakness suggestive of spinal

cord injury. In trauma patients with altered mental status, it

is best to assume that an unstable cervical spine injury is

present until proved otherwise by radiography.

B. Symptoms and Signs—Several complications of cervical

cord injury may require immediate attention and therefore

must be diagnosed promptly. Hypoventilation and respira-

tory compromise secondary to injury of cord segments sup-

plying the phrenic nerve (C3–5) usually can be diagnosed

easily and require immediate assisted ventilation. Although

respiratory dysfunction may not be apparent immediately

after a high cervical injury, respiratory status may deteriorate

during the first few days in the ICU. This can be secondary to

primary muscle fatigue or “ascending” cord involvement

from edema or ischemia. Neurogenic shock may be encoun-

tered following cervical cord injury. This results from inter-

ruption of sympathetic fibers that are descending to the

T1–L2 spinal cord segments and can lead to hypotension,

bradycardia, and hypothermia. Priapism also may occur in

males owing to unopposed parasympathetic impulses.

Although neurogenic shock patients do not appear to be

hypovolemic (eg, the skin is warm and the pulse is slow),

their hypotension responds to rapid administration of

intravascular colloid and crystalloid solutions, and use of

vasopressors such as dopamine or dobutamine is often indi-

cated to maintain arterial pressure and perfusion. Central

venous pressure and cardiac monitoring may be required

along with the frequent assessment of temperature.

After initial resuscitation, meticulous neurologic assess-

ment should be performed to determine the level and sever-

ity of spinal cord damage. Evaluation should include

assessment of motor strength; sensory testing; assessment of

reflexes, including abdominal cutaneous, cremasteric, and

bulbocavernosus reflexes; rectal and perirectal examination;

and palpation of the entire spine while the patient is carefully

log-rolled to maintain spinal alignment.

A complete spinal cord lesion is defined as total loss of

motor and sensory function below the level of injury. One

must not be confused by spinal mass reflexes such as reflex

withdrawal of an extremity in response to pain, which is not

representative of true motor function and may mistakenly

lead to classification of the injury as incomplete. Figure 31–4

portrays the motor and sensory levels of the spinal cord, and

Table 31–4 lists the important motor findings associated with

injuries at different cervical levels.

Patients with complete cervical cord lesions present ini-

tially in a state known as spinal shock, defined as a total loss of

motor and sensory function associated with an areflexic, flac-

cid trunk and extremities below the level of the lesion. In a

complete lesion, spinal shock occurs immediately after the

injury and may persist for 1–2 weeks, after which time upper

motor neuron findings develop with increased deep tendon

reflexes and increased muscular tone associated with spastic-

ity. However, abdominal cutaneous reflexes remain absent.

The mass reflex may occur and is characterized by exagger-

ated involuntary extremity movement owing to loss of

descending cortical inhibition. Interruption of autonomic

fibers results in bladder paralysis, urinary retention, poor gas-

tric emptying, and intestinal ileus with abdominal distention.

An incomplete lesion is characterized by evidence of any

motor or sensory function below the level of the lesion. In

severe incomplete injuries, spinal shock may be present ini-

tially but begins to wear off within 24 hours. Patients with

incomplete cervical cord injuries generally show some degree

of neurologic recovery (up to 40% may make a functional

recovery), whereas patients with true complete injuries

demonstrate no significant neurologic recovery. Rectal

examination is an essential part of the complete neurologic

assessment because any evidence of sacral sparing, such as

voluntary sphincter contraction or sensation in the perianal

region, classifies the injury as incomplete and implies the

possibility of some functional recovery. Important incom-

plete spinal cord injury syndromes include the following:

1. Anterior cord syndrome—This syndrome is associated

most often with cervical flexion injuries and results in loss of

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692

Spinal

nerves

Spinous processes

Medulla

oblongata

Cervical

plexus

Brachial

plexus

Sacro-

coccygeal

plexus

Filum terminale

Hearing, equilibrium

Taste

Pharynx, esophagus

Larynx, trachea

Occipital region (C1, 2)

Neck region (C2, 3, 4)

Shoulder (C4, 5)

Axillary (C5, 6)

Radial (C6, 7, 8)

Median (C6, 7, 8)

Ulnar (C8, T1)

Arm

Thorax

Femoral

region

(L1, 2, 3)

Abdomen

Epigastrium

Spine pf

scapula (T3)

Inferior

angle of

scapula (T7)

Umbilicus

(T10)

Median

Lateral

Posterior

Crural

region

(L4, 5)

Median

Lateral

SENSORY LEVELS

Intercostal

and thoracic

muscles

Lumbar muscles

Lumber plexusSacral plexus

Arm

Forearm

Hand

Abdominal muscles

Scrotum, penis

Labia

Perineum (S1, 2)

Bladder (S3, 4)

Rectum (S4, 5)

Anus (S5, C1)

Gluteal region (T12, L1)

Inguinal region (L1, 2)

MOTOR LEVELS

Facial muscles VII

Pharyngeal, palatine muscles X

Laryngeal muscles XI

Tongue muscles XII

Esophagus X

Sternocleidomastoid XI (C1, 2, 3)

Neck muscles (C1, 2, 3)

Trapezius (C3, 4)

Rhomboids (C4, 5)

Diaphragm (C3, 4, 5)

Supra-, infraspinatus (C4, 5, 6)

Deltoid, brachioradialis, and

biceps (C5, 6)

Serratus anterior (C5, 6, 7)

Pectoralis major (C5, 6, 7, 8)

Teres minor (C4, 5)

Pronators (C6, 7, 8, T1)

Triceps (C6, 7, 8)

Long extensors of carpi and

digits (C6, 7, 8)

Latissimus dorsi, teres major

(C5, 6, 7, 8)

Long flexors (C7, 8, T1)

Thumb extensors (C7, 8)

Interossei, lumbricales, thenar,

hypothenar (C8, T1)

Iliopsoas (L1, 2, 3)

Sartorius (L2, 3)

Quadriceps femoris (L2, 3, 4)

Gluteal muscles (L4, 5, S1)

Tensor fasciae latae (L4, 5)

Adductors of femur (L2, 3, 4)

Abductors of femur (L4, 5, S1)

Tibialis anterior (L5)

Gastrocnemius, soleus (L5, S1, 2)

Biceps, semitendinosus,

semimembranosus (L4, 5, S1)

Obturator, piriformis, quadratus

femoris (L4, 5, S1)

Flexors of the foot, extensors

of toes (L5, S1)

Peronei (L5, S1)

Flexors of toes (L5, S1, 2)

Interossei (S1, 2)

Perineal muscles (S3, 4)

Vesicular muscles (S4, 5)

Rectal muscles (S4, 5, C1)



Figure 31–4. Motor and sensory levels of the spinal cord. (Reproduced, with permission, from Waxman SG: Correlative

Neuroanatomy, 20th ed. New York: McGraw-Hill, 2000.)

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motor function and pain and temperature perception (ie,

corticospinal and spinothalamic tracts), with preservation of

proprioception and perception of vibration and light touch

(dorsal columns) below the level of the lesion. This is

thought to result either from direct anterior trauma or from

injury to the anterior spinal artery, which supplies the ante-

rior two-thirds of the spinal cord. The paired posterior spinal

arteries supply the dorsal columns and the posterior one-

third of the cord.

2. Central cord syndrome—This is most commonly due

to a hyperextension injury in an older patient with preexist-

ing cervical spondylosis or stenosis. The motor and sensory

deficits are greater in the upper extremities (more pro-

nounced distally) than in the lower extremities. Hemorrhagic

necrosis in the central portions (eg, gray matter) of the cer-

vical cord results in upper extremity weakness. Since the

lumbar leg and sacral tracts are peripheral in the cervical

cord, they are relatively spared.

3. Brown-Séquard’s syndrome—This syndrome occurs

with hemisection of the spinal cord, usually from penetrat-

ing injuries such as stab or gunshot wounds. The result is

ipsilateral loss of motor and dorsal column function (ie,

vibration, proprioception, and discriminatory touch)

immediately below the level of injury associated with con-

tralateral loss of pain and temperature sensation one or two

levels below the injury (spinothalamic tracts decussate

within one to two levels of their entry).

4. Posterior spinal cord syndrome—This rare syndrome

results from disruption of the posterior columns, causing

loss of vibration, proprioception, and discriminatory sense

below the level of the lesion.

C. Imaging Studies—Radiographs are essential for the eval-

uation and diagnosis of cervical spine injuries. These should

include a cervical spine series with lateral, anteroposterior,

and odontoid (open mouth) views. Radiographs are

inspected for the presence of prevertebral soft tissue swelling,

alignment of the anterior and posterior aspects of the verte-

bral bodies, angulation of the bony spinal canal, and the pres-

ence of fractures. The odontoid view is essential to diagnose

axis (C2) fractures or Jefferson fractures of the ring of the

atlas (displacement of the lateral masses of C1). Ligamentous

damage should be suspected in patients with minimal sublux-

ation or persistent neck pain without evidence of a fracture.

Dynamic flexion and extension cervical radiographs, which

should only be considered in awake and cooperative patients,

are useful to detect instability secondary to ligamentous

injury. These x-rays may be performed several days after the

initial injury so that muscle spasms, which can mask instabil-

ity by limiting subluxation, may subside.

CT scanning is excellent for visualizing the bony struc-

tures of the spinal canal and is the next step in evaluating a

fracture or subluxation. In patients with neurologic symp-

toms or signs and no radiographic evidence of bony abnor-

malities, MRI should be obtained. MRI demonstrates the

cord and soft tissue structures with outstanding clarity and

can identify intraaxial contusions and cord compression

from a herniated disk or hematoma. However, MRI does not

demonstrate bony structures very well.

The role of myelography in spinal cord injury is contro-

versial. Myelography should be performed if there is a signif-

icant incomplete neurologic deficit that cannot be explained

by bony abnormalities and if an MRI cannot be obtained.

D. Other Studies—Somatosensory evoked potentials are

occasionally useful to confirm or dispute the diagnosis of

complete spinal cord injury. This is especially true in patients

who are difficult to examine, such as those with altered men-

tal status.

Treatment

Optimal treatment of spinal cord injuries must be initiated at

the scene of the accident. The spinal cord is susceptible to

reinjury after the primary insult, making prevention of sec-

ondary injury one of the most important aims of therapy.

This includes immediate spinal immobilization with sand-

bags or a hard collar and rapid correction of hypoxia,

hypotension, shock, or hypothermia, if present. Early place-

ment of a nasogastric tube and an indwelling urinary

catheter are necessary because an atonic bladder and GI tract

commonly accompany cervical cord injuries.

Segment Important Characteristics

C1 to C3 No arm motor function. Absent respiratory muscle

contractions. If C3 is spared, patient can support neck.

C4 If the C4 segment is functional, patients may only

require initial ventilatory support and then, after

strengthening, may self-ventilate.

C5 Useful movements of the deltoid, biceps, and usually

the brachialis muscles are present, permitting shoulder

shrug, elbow flexion, and forearm pronation.

C6 Allows wrist extension.

C7 Functional upper extremity movements with maintained

innervation of the triceps (elbow extension), extensor

digitorum (finger extension), and flexor carpi ulnaris

(wrist extension). Weak finger flexors with poor grasp.

C8 Improved hand function due to innervation of most

hand intrinsic muscles.

T1 Complete hand strength maintained because of innerva-

tion of all hand intrinsic muscles.

Table 31–4. Important motor characteristics associated

with injuries at different cervical levels and T1.

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CHAPTER 31

694

Serial neurologic examinations are important to detect

signs of deterioration so that corrective measures can be

taken expeditiously. The patient must be maintained in opti-

mal physiologic condition to maximize the chances of neu-

rologic repair and recovery.

A. Respiratory Care—Patients with cervical cord injuries

frequently develop worsening of their respiratory status in

the ICU. This may be secondary to diaphragm fatigue or

ascending neurologic damage from edema or ischemia and

may require prompt respiratory support. Intubation in

patients with unstable cervical injuries should be performed

using fiberoptic nasotracheal intubation (see below for selec-

tion of neuromuscular blocking agents). Hypoventilation,

particularly during sleep, is not uncommon in the early stages

following high cervical cord injury and may require nighttime

ventilation. This is probably due to an impaired respiratory

drive to CO

or diaphragm fatigue. A high index of suspicion

for this disorder, which usually resolves in 1–2 weeks, must be

maintained in the early phases of ICU care.

Aggressive pulmonary toilet and aerosol bronchodilators

should be used to avoid atelectasis, mucus plugs, and pneu-

monia. Prophylactic antibiotics should not be used to pre-

vent pulmonary infections.

B. Hemodynamic Support—During spinal shock, decreased

sympathetic outflow may be manifested by bradycardia or

hypotension. However, one must not overlook a source of

hemorrhage (eg, liver laceration or pelvic fracture) because

such patients will not complain of pain. Hypotension from

spinal shock usually responds well to intravenous infusions

of crystalloid and colloid solutions. Vasopressors such as

dopamine may be required. Atropine, although short-acting,

may rapidly reverse hypotension associated with bradycardia.

Placement of a temporary cardiac pacemaker may be required

for severe bradycardia. Following recovery from spinal shock,

reflex hypertension, sweating, pilomotor erection, and rarely,

bradycardia or cardiac arrest (autonomic dysreflexia) may

occur. This is usually precipitated by painful stimuli such as

bladder catheterization, respiratory suctioning, or colorectal

manipulation. Hypertensive crises, which can be life-

threatening, should be treated by elimination of the precipi-

tating stimulus and administration of rapid-acting

intravenous antihypertensive agents. In recurrent severe

attacks, prophylaxis with phenoxybenzamine may be useful.

C. Cervical Immobilization—Unstable malaligned cervical

spine subluxations or fractures should be managed initially

with external immobilization. This can be achieved by

attaching tongs or a halo ring to the patient’s skull and apply-

ing distraction force through a pulley system attached to

weights. One must exclude the presence of atlanto-occipital

dislocation because traction in this condition can result in

overdistraction and serious injury. Gentle application of

5–10 lb is used initially, gradually increasing by up to 5 lb per

cervical level (eg, 20 lb for C4 and 30 lb for C6). More weight

may be required for reduction, but no more than 10 lb per

level should be administered. After each weight increase, the

lateral x-ray should be repeated to determine if realignment

has been achieved. It is often necessary to administer muscle

relaxants such as diazepam (5–10 mg intravenously every

8 hours) during skeletal traction to reduce muscle contrac-

tions or spasms that can hinder spinal realignment.

Application of a halo vest orthosis may be the proper choice

for certain bony injuries of the cervical spine.

D. Surgery—The principal goal in the management of cervi-

cal spine injuries is prevention of secondary neurologic

injury and provision of an optimal environment for recov-

ery. Securing a stable cervical spine (ie, bones, muscles, and

ligaments) will prevent further neurologic injury and reduce

the chance for persistent cervical pain resulting from insta-

bility. In general, bony lesions heal well if immobilized prop-

erly, whereas ligamentous injuries typically do not heal. The

indications for operation are decompression of incompletely

injured neural tissue and reduction and stabilization of

malaligned or unstable cervical segments. Some of the basic

features and treatment modalities for several common cervi-

cal injuries are outlined below.

1. Atlanto-occipital dislocation—These injuries, which

are seen most commonly in children owing to immature

craniovertebral articulations, are often fatal. They involve

extensive ligamentous disruption and can cause injury to the

brain stem, cervical cord, nerve roots, or vertebral artery.

Traction should not be used because it can increase the

distraction and cause further CNS damage. These injuries

are highly unstable and require operative bony fusion.

2. Jefferson fracture of the atlas—This is a burst frac-

ture of the ring of the atlas resulting from an axial force and

is usually asymptomatic. If combined displacement of the

left and right lateral masses on open mouth x-ray is more

than 6.9 mm, immobilization with a halo vest is suggested;

otherwise, a hard cervical collar is sufficient.

3. Axis fractures—A type 1 odontoid fracture involves

only the tip of the odontoid and can be treated with hard cer-

vical collar immobilization. Fractures through the odontoid

base are classified as type 2 and have a high incidence of

nonunion. Current treatment recommendations are for sur-

gical fusion if the fracture is displaced more than 6 mm or

halo vest immobilization for fractures displaced less than

6 mm. Anterior odontoid screw fixation or posterior

atlantoaxial fixation may be performed. Type 3 odontoid

fractures involve the base of the odontoid with extension into

the vertebral body and require only halo vest immobilization

for fusion. Hangman fractures are bilateral fractures of the

C2 pedicles with anterior displacement of C2 onto C3. They

are usually due to hyperextension injuries such as automo-

bile accidents in which the head hits the windshield.

Hangman fractures may be unstable and require traction ini-

tially if malalignment is present, followed by immobilization

in a halo vest. Isolated laminar or spinous process fractures

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NEUROSURGICAL CRITICAL CARE

695

of the axis usually can be treated with a hard cervical collar.

Treatment for combined atlas and axis fractures is usually

based on the type of axis fracture present.

4. Wedge compression fracture—This results from a

hyperflexion force causing compression of one vertebra

against an adjacent vertebra. The optimal management of

these injuries is controversial. Simple wedge fractures with-

out associated ligamentous injury or significant subluxation

heal well in a hard cervical collar. If the kyphotic angulation

is significant, or if instability is present, early surgical fusion

or closed realignment with skeletal traction followed by halo

vest application may be warranted. Persistent instability may

be present in 15% of patients treated by immobilization only

and requires subsequent operative surgical fusion. Care must

be taken in patients with neurologic deficits to exclude a

compressive lesion such as an extruded cervical disk that may

require early operation.

5. Flexion teardrop fracture—This is secondary to severe

hyperflexion with disruption of the intervertebral disk associ-

ated with ligamentous damage and a fracture through the

anteroinferior vertebral body. This is a highly unstable injury

often associated with devastating neurologic damage and

requires early realignment by traction. Management after initial

stabilization is controversial and may include halo vest immobi-

lization or surgical fusion. Care must be taken to exclude any

compressive lesions, such as bone or disk material, that may

contribute to neurologic dysfunction and require removal.

6. Facet dislocation—Bilateral facet dislocation occurs

when the inferior articular facet of the upper vertebra slides

forward over the superior articular facet of the lower verte-

bra. This is due to severe hyperflexion injury and is unstable.

Lateral cervical x-rays show anterior subluxation of the

superior vertebra by over 50% of the length of the vertebral

body. Anteroposterior views demonstrate alignment of the

spinous processes. Immediate closed reduction using skele-

tal traction should be attempted; if this fails, open surgical

reduction may be necessary. Surgical fusion is required in

either case. Unilateral facet dislocation results from simulta-

neous flexion and rotation injuries. The lateral cervical

spine x-ray shows anterior subluxation of the superior ver-

tebra, but this is only 30% or less of the length of the verte-

bral body. The spinous processes on anteroposterior views

are rotated and do not align. Although the unilateral locked

facet is a stable injury, it is commonly associated with nerve

root injury and chronic pain. In these patients, closed or

open reduction may be beneficial.

E. Corticosteroids—Although previous versions of this chap-

ter have advocated use of intravenous methylprednisolone

acutely after spinal cord injury, this therapy is now consid-

ered an option rather than a recommendation. Critical

analysis of the original data as well as the clinical experiences

over the past several years have not come out with significant

efficacy of this medication regime. Some clinicians may wish

to use the steroid in the hope that local nerve root improve-

ment may be hastened, but the decision needs to be weighed

against potential complications.

F. Pulmonary Embolism Prophylaxis—Pulmonary embolism

is a constant threat to patients with weak limbs and should

be combated using subcutaneous heparin (5000 units twice

daily), pneumatic compression stockings, or both.

Intravascular insertion of a vena cava filter is highly recom-

mended for patients with lower limb paralysis.

G. Gastrointestinal Considerations—Atony and paralytic ileus

may occur for days to weeks following spinal cord injury.

Early nasogastric decompression is required to reduce

abdominal distention. Serum electrolytes should be evalu-

ated regularly. Because these patients are in a catabolic state

after injury, they often require early nutritional support.

Reflex evacuation of the rectum occurs following the acute

phase of spinal cord injury and can be aided by a regular reg-

imen of laxative agents.

H. Urinary Care—Bladder atonia and sphincter paralysis result

in urinary retention after spinal cord injury. Initial placement

of an indwelling bladder catheter is required, but the catheter

should not be left in place for longer than 2–3 weeks. After this

time, reflex emptying of the neurogenic bladder can occur

spontaneously or in response to stimuli such as suprapubic

compression. Many patients require intermittent bladder

catheterization, and this can be self-administered using metic-

ulous technique. Urologic consultation is frequently helpful to

determine individual bladder care programs.

I. Skin Care—Prevention of decubitus ulcers is a primary con-

cern in spinal injury patients. Patients should be turned at

least every 2 hours, pressure points should be padded, and

kinetic therapy beds should be used if available.

J. Avoidance of Depolarizing Neuromuscular Blocking

Agents—Denervated muscles are hypersensitive to depolar-

ization, and administration of a depolarizing agent (eg, suc-

cinylcholine) can result in rapid hyperkalemia that may be

complicated by ventricular fibrillation.

Janssen L, Hansebout RR: Pathogenesis of spinal cord injury and

newer treatments: A review. Spine 1989;14:23–31.

McBride D: Spinal cord injury syndromes. In Greenberg J (ed),

Handbook of Central Nervous System Trauma. New York: Marcel

Dekker, 1993.

Ogilvy CS, Heros RC: Spinal cord compression. In Ropper AH,

Kennedy SF (eds), Neurological and Neurosurgical Intensive

Care, 2d ed. San Diego: Aspen, 1988.

Sonntag VKH, Hadley MN: Management of upper cervical insta-

bility. In Wilkins RH, Rengachary SS (eds), Neurosurgery Update

II. New York: McGraw-Hill, 1991.

Sypert GW: Management of lower cervical instability. In Wilkins

RH, Rengachary SS (eds), Neurosurgery Update II. New York:

McGraw-Hill, 1991.

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696

The term acute abdomen denotes an abdominal pathologic

condition that, if left undiscovered and untreated, would

have a deleterious effect on the patient’s health status.

Numerous factors make the diagnosis and treatment of

abdominal conditions more difficult in ICU patients.

Physiologic Considerations

The peritoneum is a complex mesothelium-lined organ that

invests the intraabdominal viscera (visceral peritoneum) and

the abdominal cavity (parietal peritoneum). The peritoneum

functions to maintain the integrity of the intraabdominal

organs and provides lubrication by peritoneal fluid (nor-

mally <50 mL). For free movement of the viscera, the nondi-

aphragmatic peritoneal surface behaves as a passive

semipermeable membrane that allows bidirectional

exchange of water and electrolytes. The diaphragmatic sur-

face is highly specialized, with numerous gaps in the peri-

toneal lining that serve as entrances to a plexus of lymphatic

channels that drain via substernal lymph nodes into the tho-

racic duct. This diaphragmatic absorptive pathway is

enhanced by respiratory excursion and normally accounts

for at least 30% of the total lymphatic drainage of the

abdomen, helping to maintain the balance between visceral

parietal transudation and parietal peritoneal fluid uptake.

The omentum participates in absorption of peritoneal

fluid and particulate material up to 10 μm in diameter. The

omentum is highly mobile and can act to seal off a perforated

viscus or contain a bacterial inoculum.

Pain from intraabdominal disease is transmitted via

somatic sensory and visceral autonomic pathways. Visceral

pain, primarily elicited by distention, is referred in a logical

fashion in the same order as embryologic development; the

nerves accompany the major splanchnic vessels. Foregut

sources (eg, esophagus, stomach, liver, pancreas, biliary tract,

duodenum, and spleen) elicit upper epigastric pain, midgut

lesions (eg, jejunum, ileum, appendix, and right colon) elicit

periumbilical pain, and hindgut lesions (eg left colon and rec-

tum) radiate to the hypogastrium. This visceral pain is typically

colicky in nature and somewhat vague in location—in con-

trast to somatic pain, which is usually constant and well local-

ized to the site of direct parietal peritoneal irritation.

Intraabdominal disease also can cause pain to be referred

to other areas through neural pathways or other anatomic

constraints. Examples of referred pain include shoulder pain

from splenic or hepatic hemorrhage, causing phrenic nerve

irritation, and hip or thigh pain from a psoas abscess.



Pathophysiology

Critical care patients are susceptible to common causes of

abdominal disease such as appendicitis, diverticulitis, and

calculous cholecystitis with approximately the same fre-

quency as the general population. More important, they are

prone to develop more complex and unusual abdominal

processes resulting from a variety of predisposing condi-

tions. For example, recent surgery, especially involving

enteric anastomoses, may lead to intraabdominal abscess or

small bowel obstruction.

Shock with associated low flow states leads to an

increased risk of mesenteric ischemia, acalculous cholecysti-

tis, and possibly gut translocation of bacteria. Present or pre-

vious antimicrobial therapy also may contribute to illness

with overgrowth of resistant organisms, including Clostridium

difficile (pseudomembranous) colitis. The fasting state of

many critically ill patients may contribute to the develop-

ment of acalculous cholecystitis or, along with opioid use,

lead to a colonic pseudo-obstruction (Ogilvie’s syndrome;

see below).

Iatrogenic complications are common in patients under-

going multiple procedures and receiving several medications.

Inadvertent visceral injury may occur during paracentesis or

thoracentesis. Missed intraabdominal disease in traumatized

patients should be strongly considered in any patient not

recovering as expected. The problem of stress gastritis and

stress ulcers has been diminished with aggressive pH moni-

toring and pharmacologic prophylaxis but still presents a

formidable challenge.

Acute Abdomen

Allen P. Kong, MD

Michael J. Stamos, MD