Файл: NMS Surgery_booksmedicos.org.pdf

Thus, pupillary dilatation is more reliable in localizing the lesion. In 20% of the cases, the pupillary dilatation is opposite and hemiparesis is ipsilateral to the lesion—a false localizing sign known as the

Kernohan -Woltman notch phenomenon (Kernohan's notch).

Transforamen magnum herniation. The cerebellar tonsils herniate through the foramen magnum. The resulting medullary compression may elicit a Cushing's response (i.e., hypertension, bradycardia, and apnea) and ultimately leads to death.

D Cerebral blood flow, autoregulation, and CPP

Overview (Fig. 27 -2)

The average cerebral blood flow normally ranges between 50 and 55 mL/100 g of brain tissue per minute , with the gray matter having a higher flow (i.e., 75 mL/100 g/minute) than the white matter (25 mL/100 g/minute).

The blood flow is coupled to the local metabolic demands and is highest where the density of synapses is greatest (termed metabolic autoregulation ).

The flow is directly proportional to the mean arterial pressure (MAP) and the vessel radius (r)(Q

MAP × r4 , Poiseuille's law ), and it is inversely proportional to the blood viscosity and vessel length. These factors can be manipulated to improve cerebral blood flow.

Pressure autoregulation describes the observation that normally over a wide range of mean arterial pressure (50–150 mm Hg), the cerebral blood flow remains unchanged at 50 mL/100 g of brain tissue per minute (Fig. 27 -2).

This may change focally or globally as a result of head injury, subarachnoid hemorrhage (SAH), stroke, or a brain tumor.

P.504

FIGURE 27-2 Cerebral blood flow versus cerebral perfusion pressure. Note that normal autoregulation that occurs for cerebral perfusion pressure is 50–150 mm Hg.

In the patient with intact autoregulation, ICP remains stable as blood pressure changes within the limits above.

However, if the ICP passively follows the arterial pressure, it is indicative of impaired autoregulation

Lesions in the midbrain can cause central neurogenic hyperventilation (deep breathing at a very fast rate) that may lead to severe alkalosis.

Lesions in the lower pons can cause apneusis , which is complete cessation of involuntary breathing, leading to respiratory arrest during sleep (Ondine's curse).

Medullary lesions can lead to various types of abnormal breathing patterns, which include:

Cluster breathing (a disorderly sequence of clusters of breaths with irregular pauses)

Ataxic breathing (Biot's breathing—periodic breathing in which apneic periods are punctuated by a few irregular deep breaths, lacking the waxing and waning pattern of Cheyne - Stokes respiration)

Cheyne -Stokes respiration (see IV B 4 b)

Gasping (breathing in which both deep and shallow breaths occur randomly with haphazard intervening pauses and a slow respiratory rate, which may finally lead to apnea)

Kussmaul's respiration , deep rapid breathing similar to central neurogenic hyperventilation, usually occurs as a result of diabetic or uremic acidosis.

C Neurologic evaluation

A detailed neurologic evaluation may not be possible in some emergency situations, and a brief examination will have to suffice to assess the neurologic damage.

The level of consciousness should be determined first. Patients may present as:

Alert, awake, and oriented

Lethargic (i.e., sleepy but easily arousable)

Stuporous (i.e., responsive only to noxious stimuli)

Comatose (i.e., not responsive to noxious stimuli)

Examination of the pupils. The pupils are examined for their size and reaction to light, and the position and movement of the eyes are noted. A few general rules may be helpful in localizing a lesion.

When a lesion in the cortex is present, the size of the pupil may be 6 mm or larger, and there may be wandering or roving eye movements.

With a lesion in the basal ganglia , the pupils may range from 2–3 mm in size, and the eyes are deviated downward and inward.

A lesion in the midbrain may be associated with pupils that are 4–5 mm in size (midrange), and convergent nystagmus or nystagmus retractorius may be present.

A lesion in the pons may be associated with pinpoint pupils (1 mm) and with ocular bobbing.

When a lesion in the medulla is present, the pupils may be slightly small (2 mm), and there is downbeat nystagmus.

Brain stem reflexes , such as the oculocephalic (doll's eye) reflex and the caloric (oculovestibular) responses, are checked to rule out irreversible brain stem damage.

Motor examination is then performed. In a comatose patient, it may only be possible to assess the response to painful stimuli.

Sensory level determination is important in patients with spinal cord lesions (see VI E 3).

Deep tendon reflexes and plantar responses are checked to distinguish a lower motor neuron lesion from an upper motor neuron lesion.

V Head Injuries

A Incidence

Trauma is the leading cause of death in the United States in people between the ages of 1 and 44 years. In nearly 75% of all trauma -related fatalities, head injury contributes significantly to the outcome. Approximately 60,000 patients with severe head injuries reach a hospital alive each year; an equal number of patients die before receiving hospital care.

Prevention is the most important area of intervention in head trauma.

Drunk driving, as well as failure to use safety belts or motorcycle helmets, significantly contributes to the severity of head injury.

Care of the severely head-injured patient begins at the scene of the accident.

P.506

To prevent serious exacerbation of brain injury, it is essential to establish a secured airway, provide adequate ventilation, and support the circulation.

Hypoxia, hypercapnia, and hypotension must be corrected.

Hypotonic intravenous solutions (e.g., 5% dextrose in water) must be avoided because they promote an osmotic gradient between the intravascular compartment and brain interstitial space, causing traumatic cerebral edema. Colloid solutions, such as albumin and blood products, are preferred.

B Classification

Brain injuries occurring after trauma can be classified as:

Primary, occurring instantaneously at the time of impact

Secondary , resulting from a chain of events triggered by the initial injury. If not controlled, secondary injuries lead to further damage through ischemia, hypoxia, or both.

Primary and secondary injuries can be either:

Nonhemorrhagic focal or diffuse edema

Hemorrhages

Intra -axial (i.e., intracerebral; within the brain substance)

Extra -axial (i.e., extracerebral; outside the brain parenchyma, such as epidural and subdural

hematomas)

C Initial management and assessment

Immediate care of a head trauma victim is not different from that of any other injured patient.

Priorities (A, B, C)

Establishment of adequate airway and ventilation (A—airway)

Control of hemorrhage (B—bleeding)

Maintenance of peripheral vascular circulation (C—circulation)

Volume replacement with colloids or blood products can be performed when necessary to reduce the risk that cerebral edema will develop or worsen.

Stabilization of the neck with a hard cervical collar is necessary in all patients.

10% of patients with severe head injuries have associated spinal cord injuries; thus, all patients with head injuries should be transported using SCI precautions.

Precautions include immobilization of the entire spine on a full spine board and use of a cervical collar.

Blood is drawn for typing and cross matching and for other laboratory studies.

Initial examination

The type and magnitude of the injuries can be determined by information gleaned from the initial examination. For example:

A closed -head injury—injury inflicted to the brain without any evidence of scalp laceration

An injury resulting from a high -speed, nonimpact acceleration–deceleration

Blunt trauma with or without a scalp laceration or contusion (all scalp lacerations should be checked manually for an underlying skull fracture)

A penetrating wound from a knife or a bullet (entrance and exit wounds must be sought)

Location of a fracture can be determined by certain signs.

Fractures traversing the base of the skull (basilar fractures) often cause ecchymosis behind the ear (Battle's sign) and may be associated with otorrhea.

Anterior basal fractures often result in periorbital ecchymosis (raccoon's eyes) and subconjunctival hemorrhage and, if associated with cribriform plate fracture, may result in rhinorrhea.

Hematotympanum is associated with fracture of the petrous ridge.

History. After the initial management, and if the patient is awake, a quick history should be obtained.

Severity of head injury and final outcome are directly related to the duration of unconsciousness, which the history may reveal.

Neurologic evaluation. A rapid assessment of the patient is performed.

P.507

The Glasgow Coma Scale (GCS) is now used almost universally in the assessment of the head-injury victim (see Table 21 -2). Motor responses, eye responses, and verbal responses are measured.

The GCS score ranges from 3–15.

The GCS score at 6 hours after trauma is a good predictor of the long-term outcome in head injury (i.e., recovery, disability, vegetative state, or death).

Adult patients with a 6-hour GCS score below 7 are likely to have a poor outcome; the prognosis is much better in the pediatric population.

Coma is defined as GCS score lower than 8.

Neurologic examinations are repeated periodically; a change of 2 or more in the GCS score is considered significant.

Radiographic studies

Computed tomography (CT) scans are preferable to skull radiographs in severely injured patients.

Diagnostic findings

Hematomas (see VII B 1–2) can be easily diagnosed because acute blood appears, relative to the brain:

Hyperdense if hemoglobin >9 mg/dL

Isodense if hemoglobin = 9 mg/dL

Hypodense if hemoglobin <9 mg/dL

Epidural hematomas appear as semilunar (“lenticular”) dense collections with a convexity toward the brain.

Acute SDHs have a concavity toward the brain and conform to the shape of the brain surface.

Cerebral edema can be assessed by the size of the ventricles, basal subarachnoid cisterns, loss of gyral pattern, and degree of midline shift.

If the CT scan is positive, the patient is taken immediately to the operating room for evacuation of hematomas or to the intensive care unit for ICP monitoring and management of brain swelling.

In a patient with significant neurologic deficits, MRI brain scan may show brain injury when a CT head scan result is normal.

Locations of shearing injuries (white matter edema and disruption) are imaged better with MRI scan than CT scan.

Diffuse shearing injuries are frequently located in the corpus callosum, subcortical white matter, thalamus, and brain stem.

Radiographs of the cervical spine are taken to rule out associated spinal injuries.

The presence of cervical spine fracture or neurologic deficit referable to cervical spine is an absolute contraindication for removal of immobilization devices (cervical collar) or performance of flexion/extension views.

Cervical spine series is incomplete until C-1 to T -1 levels are adequately visualized.

In the absence of cervical fracture or cervical spinal cord deficit, flexion/extension views of the cervical spine are required to rule out ligamentous injury.

In the patient who has been comatose for longer than 2 weeks, an MRI of the cervical spine can be useful to perform lateral or flexion/extension views to rule out occult ligamentous injury, disc herniation, or SCI.

D Management of increased ICP

Maintenance of an adequate CPP to prevent irreversible ischemic injury is the major goal of treatment of increased ICP. The patient's CPP is maintained above 50 mm Hg by manipulation of the ICP and the MAP.

Placement of an ICP monitor is necessary to evaluate status and ICP therapy in the unconscious patient.

Criteria for placement of an ICP monitor include one or all of the following:

A GCS score of less than 8. In practical terms, for the intubated, unconscious patient, ICP monitoring is usually needed when the best motor response is decorticate or decerebrate posturing or flaccid.

P.508

Associated systemic complications, such as severe hypotension or hypoxia

CT evidence of diffuse cerebral swelling , especially with obliteration of perimesencephalic cisterns, indicating limited residual compliance and minimal tolerance to further brain swelling

ICP measuring devices (monitors) are of three types:

Intraventricular catheter (ventriculostomy) gives the most accurate measurement and allows removal of CSF to lower the ICP in an emergency. Placement of an intraventricular catheter can be difficult in the presence of diffuse brain swelling with slitlike ventricles.

Subarachnoid bolts (Richmond screw or Philly bolt) are easy to place, give accurate readings, and are associated with a low infection rate.

Intraparenchymal monitors

These devices are fiber -optic ICP probes and are useful when a ventriculostomy catheter cannot be placed.

The intraparenchymal monitor is also useful for superficial cortical monitoring in patients with consumptive coagulopathy, thus reducing risk of hemorrhagic complication of a more deeply placed ICP monitoring probe.

Intracranial hypertension can be managed by a variety of methods. The following therapies can be used in sequence.

Elevation of the patient's head promotes venous drainage, thereby decreasing ICP.

Hyperventilation is used in patients with GCS score greater than 5. The cerebral vessels respond quickly to a change in the arterial Pco2 . A low Pco2 causes vasoconstriction, thus reducing the blood component of the intracranial volume, whereas an elevated Pco 2 causes vasodilation.

The Pco2 is maintained between 22 and 28 mm Hg. Hyperventilation is not a long-term option for ICP control.

If the ICP is not sufficiently lowered by hyperventilation, other therapies have to be used, such as:

Hyperosmolar agents

Loop diuretics

Barbiturates

Increasing the serum osmolality (to approximately 300–310 mOsm)

Hyperosmolar agents

The diuretic most commonly used is mannitol, which is administered intravenously to adults in a bolus of 1.0 g/kg followed by infusion of 25–50 g every 4–6 hours. Its effect can be seen in 5–20 minutes.

A combination of albumin and loop diuretics (furosemide) has been shown in experimental studies to be superior to mannitol for achieving reduction of cerebral edema.

Serum osmolality and electrolytes have to be measured every 6 hours.

Mannitol should be held for serum osmolality greater than 310 mOsm/L, and systolic blood pressure less than 110 mm Hg.

Loop diuretics. Furosemide is the drug most commonly used and is administered intravenously. The effect of the drug is rapid.

Barbiturates may be used if all of the previously mentioned efforts fail to lower the ICP.

An initial dose of 3 mg/kg of sodium pentobarbital is given intravenously, followed by a maintenance dose of 0.5–3 mg/kg/hour. The effect of the drug occurs within minutes. A burst suppression pattern on compressed spectral array electroencephalogram consisting of 3–6

bursts per minute suggests that a therapeutic response has been reached. It is not useful to monitor serum barbiturate levels.

Barbiturates cause myocardial depression and loss of vascular tone, which lead to hypotension, and vasopressor agents may be necessary to elevate the MAP to maintain an adequate CPP.

Although the exact mechanism of action is not known, barbiturates may act by:

Decreasing cerebral blood flow

Reducing the metabolic activity and nutritive demands of the brain

Reducing synaptic transmission

P.509

All patients undergoing barbiturate coma therapy should have a Swan -Ganz catheter placed to measure cardiac pressures and optimize cardiac output.

Hypothermia may be used as an adjunct to other therapies. The core temperature of the body is lowered from normal to a temperature that ranges from 32°C–34¼°C. This method probably decreases the ICP by reducing cerebral metabolism.

Complications of hypothermia include cardiac depression below 32¼°C.

An increased incidence of infectious complications (e.g., pneumonia) has been reported with hypothermia therapy.

Consumptive coagulopathy

Severe parenchymal brain injury causes release of tissue thromboplastin, which activates the extrinsic clotting pathway.

Diffuse intravascular fibrinolysis ensues, completing disseminated intravascular coagulation and fibrinolysis, due to head injury.

The complete clinical syndrome is diagnosed with extended prothrombin time (PT) and activated partial thromboplastin time (APTT) values, decreased fibrinogen level, elevated fibrin split products, and decreased platelet count.

Extended PT and APTT are treated with fresh frozen plasma.

Fibrinogen levels below 150 mg/dL require cryoprecipitate for treatment.

Platelet packs should be given to treat head-injury patients with a platelet count less than 100,000/mL if the bleeding time is extended.

Post -traumatic epilepsy. Risk of post-traumatic epilepsy correlates with severity and location of underlying brain injury. Failure of cerebral perfusion can occur when seizure activity is superimposed on the injured brain.

Patients who are at risk for early post-traumatic epilepsy include those with:

Intracranial hematoma

Supratentorial depressed skull fracture

Brain injury with focal neurologic signs or post-traumatic amnesia for more than 24 hours

Combat missile wounds

Prophylaxis for patients at risk, including those who have experienced more than one seizure due to head injury and patients in the high-risk categories mentioned above, is phenytoin (1.0 g intravenously [not to exceed 50 mg/minute] or by mouth as loading dose, followed by 300 mg per day, or as needed for therapeutic serum level). Dose for children is 10 mg/kg initially, followed by a maintenance of approximately 5 mg/kg per day.

E Management of intracerebral hematomas and cerebral contusions

Intracerebral hematomas result from the tearing of small vessels in the white matter and are due to penetrating trauma or acceleration–deceleration injuries.

Cerebral contusions. Superficial hemorrhages most commonly occur when the anterior temporal and frontal lobes strike the rough edges of the tentorium or skull.

A coup injury occurs when the skull strikes the brain underlying the site of impact.

A contrecoup injury occurs directly opposite to the impact site when the brain strikes the inner table of the skull on the opposite side along the force vector. Thus, if a person were struck on the back of the head, the coup injury would be to the occipital lobe and the frontotemporal tips would sustain the contrecoup injury.

Surgical decompression of intracerebral hematomas and cerebral contusions may be necessary when increased ICP (caused by a mass effect from the accumulated blood and the secondary edema) becomes refractory to medical management.

F Management of scalp injuries

The scalp is made up of five layers:

S ––skin

C––dense subcutaneous tissue

A––aponeurosis

P.510

L ––loose areolar tissue

P ––pericranium

The scalp is highly vascular, and much blood can be lost from scalp lacerations before they are sutured.

The scalp wound is thoroughly cleansed, debrided, and sutured as soon as possible.

Any laceration larger than 6–8 inches should be closed in the operating room.