2. Pharmacy
Several drugs are part of the "routine" surgical and medical management of head injury. These include antibiotics, anticonvulsants, B-vitamin cocktails, vitamin K, and alcohol drips (but not steroids). Pentobarbital is infrequently used partially because of its disproportionately complicated supportive care requirement.
2.1) Antibiotic
Many neurosurgeons keep patients perioperatively on 24 hours of a broad-spectrum cephalosporin, penicillin, or other antibiotic. Antibiotics should be most strongly considered in cases of known or suspected (on the basis of injury mechanism) intradural contamination.
2.2) Anticonvulsant
Posttraumatic seizures occur most frequently in those head injured patients found to have 1. Acute subdural hematomas and 2. subcortical intraparenchymal hematoma (traumatic contusion or hemorrhage) in epileptogenic (ie. potential seizure initiation) focus. Anticonvulsant blood levels should be checked on a schedule based on its half life and other pharmacodynamic characteristics.
TABLE: Anticonvulsants and head injury
| Anticonvulsant |
Half life |
Dose to start |
Time from first dose to reach steady state level (Time to draw first level after bolus) |
| Phenytoin |
dfg |
dfg |
dfg |
dfg |
| Phenobarbital |
dfg |
dfg |
dfg |
dfg |
2.3) Vitamin K
A cofactor for the vitamin K-dependent hepatic-produced clotting factor enzymes. Should be given to any patient who by laboratory criteria or clinical suspicion (alcoholic, stigmata of liver failure, history of bruising, nose or other bleeding) has a bleeding diathesis.
2.4) B vitamin cocktail
A large percentage of head injured patients (including those requiring craniotomy for clot evacuation) are drunk at the time of injury. Many head injured patients are chronic alcohol abusers. Vitamin B deficiency is a frequent accompaniment of long term abuse and can be associated with neurologic signs (ophthalmoplegia, confusion, etc.) that overlap with those of head injury.
2.5) Alcohol drip
Among chronic alcoholics and drug abusers suddenly deprived of substances that their nervous and systemic physiology have accommodated to slowly over many years or even decades of abuse a significant number will show signs of alcohol withdrawal, namely: autonomic aberrations, delirium tremens, etc.)
1.4) Fever
Fever is a sign of infection For every degree centrigrade fever there is a __% increase in metabolic rate which puts further stress on oxygen supply and delivery mechanisms.
Management of fever in the head injured patient is based on two considerations: attempting to control the deleterious effects of the temperature elevation itself as well as determining and dressing the agent that incited the pyretic pathophysiologic cascade.
Cooling measures include alcohol and ice baths as well as cooling blankets.
A fever workup should be promply initiated for patients with temperature greater than 101.5 degrees. The workup includes urinalysis with cultures and sensitivity, and sputum culture
The post operative period begins once the dressings are applied and the drapes removed. It continues through the immediate acute post operative period (in which management concerns are those of life support), into the acute but stable period (where nutrition and extended venticulostomy management, as well as management of nosocomial pneumonias and prevention of venous stasis thrombosis are priorities). In the subacute post op period In the extended post operative period the principal issues are no longer medical or surgical (with the exception of occasional issues of cosmesis), but functional and social (rehabilitation).
I. Immediate acute (0 to 36 hours)
The patient should not be transferred out of the operating room unless and until the surgeon is convinced that there is no residual, recurrent, or newly evolving lesion requiring further operative intervention. Surgeon and anesthesiologist should consult prior to removal of the patient from the OR to the ICU.
If at all possible, the person administering anesthesia should titrate dosage and time administration of paralyzing and sedating medications such that these will have worn off by the time the surgeon completes application of the head dressing. The surgeon needs to be able to assess the patient's neurologic status (ability to move, level of consciousness, etc.) as soon as possible post-op to determine if more surgery or imaging is immediately required. Long-acting paralytic medications such as pancuronium should be discontinued at least one hour prior to the end of surgery. Short-acting or readily reversible narcotic agents are useful for sedating the patient when surgery runs longer than expected.
The surgeon should reconsider transfer directly from the OR to the ICU if the patient has pupillary asymmetry or a focal deficit not present prior to surgery. As he checks the pupillary response the surgeon should remember that it differs in each of the stages of anesthesia: pinpoint pupils which otherwise would be consistent with pontine dysfunction are normal in the deepest stage of anesthesia and will enlarge as the patient's anesthetic lightens. Fixed and dilated pupils (single or pair) are not normal in any stage of anesthesia.
In the event that the patient has a new focal deficit (including a "blown" pupil) the surgeon has the option of getting an immediate emergency head CT or of remaining in the OR and re-prepping, draping, and re-opening the scalp and bone flap to inspect and explore the site from which the hematoma was evacuated. Immediate re-expoloration should be done only if 1. the patient's vital signs are consistent with a Cushing response (hypertension and bradycardia) and 2. a CT scanner is not readily available.
The patient should not be transferred with any compromise of hemodynamics, ventilation, or airway control. If the patient is not breathing spontaneously the cause may be pharmacologic or neurologic. A combination of post traumatic neurologic compromise and opiate drugs is often the cause of slowness of the patient to breathe unassisted while emerging from anesthesia after a head trauma craniotomy. An ampoule of the very short acting opiate antagonist naloxone can be given to accelerate emergence from anesthesia, remembering that if this is effective it will have to be followed by subsequent repeat doses for the remainder of time required for metabolism of the anesthetic opiate.
Hypertension can contribute to post-operative bleeding particularly into a parenchymal cavity after evacuation of an intraparenchymal hematoma. Intravenous anti-hypertensive medication or a sedative (the latter if the patient is bucking against the endotracheal tube) can usually keep the pressure under control for transfer. In the face of refractory hypertension, the ICU should be alerted to have a nitroprusside drip ready on the patient's arrival there.
Patients should be physiologically monitored during transport following head trauma craniotomy. Sudden shifts of intracranial contents (herniation) or rapid increases in intracranial pressure (malignant brain swelling) are common sequelae to head injury in the acute post- as well as pre-op period. Physiologic parameters that would be expected to alter with a classic Cushing response (bradycardia, hypertension, irregular respirations) should be monitored during transport from the OR to the ICU.
1.4) Fever
Fever is a sign of infection For every degree centrigrade fever there is a __% increase in metabolic rate which puts further stress on oxygen supply and delivery mechanisms.
Management of fever in the head injured patient is based on two considerations: attempting to control the deleterious effects of the temperature elevation itself as well as determining and dressing the agent that incited the pyretic pathophysiologic cascade.
Cooling measures include alcohol and ice baths as well as cooling blankets.
A fever workup should be promply initiated for patients with temperature greater than 101.5 degrees. The workup includes urinalysis with cultures and sensitivity, and sputum culture
2. Pharmacy
Several drugs are part of the "routine" surgical and medical management of head injury. These include antibiotics, anticonvulsants, B-vitamin cocktails, vitamin K, and alcohol drips (but not steroids). Pentobarbital is infrequently used partially because of its disproportionately complicated supportive care requirement.
2.1) Antibiotic
Many neurosurgeons keep patients perioperatively on 24 hours of a broad-spectrum cephalosporin, penicillin, or other antibiotic. Antibiotics should be most strongly considered in cases of known or suspected (on the basis of injury mechanism) intradural contamination.
2.2) Anticonvulsant
Posttraumatic seizures occur most frequently in those head injured patients found to have 1. Acute subdural hematomas and 2. subcortical intraparenchymal hematoma (traumatic contusion or hemorrhage) in epileptogenic (ie. potential seizure initiation) focus. Anticonvulsant blood levels should be checked on a schedule based on its half life and other pharmacodynamic characteristics.
TABLE: Anticonvulsants and head injury
| Anticonvulsant |
Half life |
Dose to start |
Time from first dose to reach steady state level (Time to draw first level after bolus) |
| Phenytoin |
dfg |
dfg |
dfg |
dfg |
| Phenobarbital |
dfg |
dfg |
dfg |
dfg |
2.3) Vitamin K
A cofactor for the vitamin K-dependent hepatic-produced clotting factor enzymes. Should be given to any patient who by laboratory criteria or clinical suspicion (alcoholic, stigmata of liver failure, history of bruising, nose or other bleeding) has a bleeding diathesis.
2.4) B vitamin cocktail
A large percentage of head injured patients (including those requiring craniotomy for clot evacuation) are drunk at the time of injury. Many head injured patients are chronic alcohol abusers. Vitamin B deficiency is a frequent accompaniment of long term abuse and can be associated with neurologic signs (ophthalmoplegia, confusion, etc.) that overlap with those of head injury.
2.5) Alcohol drip
Among chronic alcoholics and drug abusers suddenly deprived of substances that their nervous and systemic physiology have accommodated to slowly over many years or even decades of abuse a significant number will show signs of alcohol withdrawal, namely: autonomic aberrations, delirium tremens, etc.)
1.5) Hematology
The major hematologic management issues following severe head injury are the indications and appropriate components for blood product transfusions as well as the indications, route of administration, and agent of choice for the prevention of thromboembolism.
Red blood cell transfusions in either a pure concentrate or whole blood preparation are reserved, as noted above, for patients who have low hematocrit with vital signs changes suggestive of decreased oxygen delivery and hypovolemia.
Platelet levels can drop from dilution following transfusions of large volumes (more than 4 to 5 units) of packed red cell preparations with platelets filtered out.
Fresh frozen plasma is another product that should be replaced (according to the prothrombin level) concomitant with the transfusion of large volumes of packed cells washed of their clotting factors. Cryoprecipitate is the agent of choice for many kinds of hemophiliac and for the treatment of DIC.
TABLE: Post craniotomy blood products and transfusion indications
| COMPONENT |
THRESHOLD |
MONITORING |
| Packed red blood cells |
Hematocrit < 25% (bleeding transient and/or slow) |
Hematocrit |
| Fresh frozen plasma |
PT < |
PT |
| Platelets |
Platelet count (stigmata: ecchymosis, gum bleeding) |
Platelet count |
| Cryoprecipitate |
PT < |
PT |
| Whole blood |
Hematocrit < 25% (protracted continuous exsanguination) |
Hematocrit, platelet count, PT |
a) Anticoagulation
Anticoagulation is part of prophylaxis against formation of venous stasis thrombi which are liable to form in the immobile lower extremities of patients comatose following a head injury or paraparetic (or -plegic) following a spinal cord injury. Prophylaxis of DVT by the administration of "mini"-dose heparin has never been demonstrated to decrease the incidence of DVT in head injured patients. Patients should not be started on coumadin until 48 hours post head trauma craniotomy (or even placement of a ventriculostomy) if the likelihood of developing a fatal thromboembolism is any more imminent than remote.
1.6) Comfort
Sedation should be continued as long as necessary to keep the patient's lines in place and dressings intact. Agents that are readily and reliably reversible such as morphine or meperidine (Demerol) are good sedating agents as is the very short acting agent propofol which can be turned on and off as needed.
TABLE Post op sedation and comfort medications
| MEDICATION |
ADMINISTRATION/DOSING |
LASTS |
EFFECT/EXAM |
REVERSAL |
| Morphine |
IV 2-4 mg
IM |
?-1 hour |
Sedation, respiratory depression |
dfg |
| Demerol |
IV
IM |
dfg |
Sedation, respiratory depression |
dfg |
| Fentanyl |
IV |
dfg |
dfg |
dfg |
| Etomidate |
IV |
dfg |
dfg |
dfg |
| Propofol |
IV |
dfg |
dfg |
dfg |
| Haloperidol |
IV |
dfg |
dfg |
dfg |
1.7) Cervical collar
Patients whose necks have not been cleared prior to surgery can be cleared postoperatively according to an algorithm such as the one that follows:
TABLE: Clearance of the cervical spine
Three stages:
1. Identify patients at risk
Patients with unstable vertebral columns are a subset of patients with cervical bone or soft tissue injuries which is a subset of all patients with either a mechanism, a neurologic finding, or a complaint (pain) suggestive of a cervical spine injury.
a. Mechanism
b. Neurologic finding
c. Pain
2. Identify anatomic abnormalities
3. Rule out instability
Acute (up to five days) post op care begins as soon as the patient arrives in the ICU. At this time many post-head trauma craniotomy patients continue to require a multiplicity of tubes, lines, machines, and intensive care nursing for life support and physiologic monitoring.
Wound care after an uncomplicated trauma craniotomy is straightforward: drains are discontinued within a day or two, dressings are changed once or twice before being removed (usually on the 3rd or 4th post operative day), and by day 7 staples or sutures approximating the skin can come out.
During the subacute postoperative period (five days to two weeks) indolent infections and more slowly evolving pathophysiologic processes become evident. Long term post op care (two weeks to two years) is given in the hospital, at home, and in the community and is primarily associated with the rehabilitation of the head trauma victim.
TABLE Post op orders
| ORDER |
INSTRUCTIONS |
| Admit |
To ICU |
| Diagnosis |
S/p operation name |
| Condition |
condition |
| Vitals |
Q 1h with neuro checks |
| Allergies |
allergies |
| Activities |
bedrest |
| Nursing |
Ventriculostomy
Arterial line
CVP line
JP Foley |
| Diet |
sdf |
| Medications |
Antibiotic
Anticonvulsant |
| IV |
sdf |
| In and out |
sdf |
| Labs |
sdf |
1. Dressings
The head dressing should be inspected each day post operatively until it is removed on the third post op day. In order to examine for soiling or leakage posteriorly the patient's head should be carefully lifted off of the pillow and turned to the side. The integrity and cleanliness of a head wrap cannot be assessed from the foot of the bed or across the room.
Head dressings should not be disturbed for the first twenty four hours unless inordinate bleeding requires that they must. A small amount of post operative ooze from freshly closed skin incision may be present by the time the patient is delivered from the OR to the ICU. At this time the border of the blood stain on the dressing should be traced with a pen, dated and timed. At regular intervals thereafter the same marking is performed such that the extent and rapidity of continued bleeding can be tracked.
Blood soaks through a head dressing if there are gaps between the points of approximation of the wrapping gauze or if the overlap is too little. It is the fault of the surgeon on closure of either or both galea and skin. Even a transected scalp artery should not continue to bleed after skin closure if the galea is tightly brought together and sutures or staples have been placed at close enough intervals. The surgeon should be no more embarrassed about having to remove a head dressing to identify the site of incision leakage than he was about allowing it to leak in the first place.
If only a small amount of blood leaks through the stained area should be covered with a few clean gauze sponges taped in place. This does nothing to stop the leakage but makes the dressing less visually upsetting to nurses and visitors until the first dressing change. Soakage that overwhelms the absorptive capacity of two or three sponges suggests bleeding from the wound that is not stopping on its own and which therefore threatens complications as anemia and infection.
A head dressing should be removed as a two person procedure. The patient's head is liable to flop around if the surgeon is at the same time attempting to hold it off of the bed and cut it. An assistant should hold the patient's head while the surgeon cuts the dressing. Even turban-type dressings should be cut rather than unwrapped for patient safety as well as surgeon convenience. Before cutting a head dressing make sure that no plastic tubes or electrical wires have been taped to it and lay in the cutting path.
If bleeding is detected at a specific site along the incision a simple skin suture (not buried) should be placed. Bleeding from an extended segment requires a running suture.
If they remain clean and dry, the original head dressings put on at the end of the craniotomy should be left in place for two to three days. After a few days the wound under the most pristine head wrap should be inspected for signs of infection (rubor, calor, tumor, and dolor), as well as for areas of non-viable, necrotic skin.
A dusky, bluish tinge to the skin edge suggests nonviable tissue and may not be unexpected if a complex laceration repair was required at the time of craniotomy. A few sponges should be placed over the area to provide tamponade until a later time when the wound can be revised.
Scalp staples or sutures should be left in from five to seven days after a craniotomy with a new skin incision. If a pre-existing scar has been opened healing will be slower and staples should be left in seven to ten days. The 5-0 nylon sutures used to sew up facial laceration should be removed three days after placement at which time steri-strips can be laid across for further healing.
2. Drains
Drains should be removed within twenty four hours lest they become conduits of infection. Twenty milliliters per 8-hour shift or less of drainage is little enough that the drain can be safely removed without inordinate risk of re-accumulating of intracranial hematoma. After forty-eight hours, the drain should come out regardless of output. If greater than 30 cc per shift of fluid is still draining two days post op, there is a potential problem. Start the workup with a CT of the head.
If the drains have not been sewn in (as recommended in the chapter on generic craniotomy techniques) they can be pulled out without taking off the head wrap. The Jackson Pratt suction bulb should be opened prior to removing the intracranial portion of the drain.
Post operative intensive care monitoring following head injury craniotomy must be extensive enough to detect changes in neurologic and systemic parameters that would require medical or surgical intervention.
1. Systemic
Non neurologic, systemic monitoring must at a minimum address hemodynamic, ventilatory, and metabolic pathophysiology seen in association with head injury severe enough to require a head trauma craniotomy.
1.1) Perfusion
Hemodynamic monitoring may be as simple as following urine output and measuring blood pressure, but where fluid balance and volume status are a control a central venous catheter should be placed. If cardiac contractility is an issue, the patient should be monitored with a Swan Ganz catheter.
1.2) Ventilation
Ventilation is monitored anatomically with serial chest x-rays, blood gases, and pulmonary function tests. Adjustments in tidal volume, IMV, PEEP, and FIO2 should be titrated to pCO2, pO2, pH, and O2 saturation of the blood at serial intervals of 6 to 12 hours for the first 48 hours post op.
1.3) Metabolism
Because of variations in individual physiology, lesion, and intraoperative course, there are no "routine" labs, nor a schedule for repeating labs following craniotomy for head trauma appropriate for all patients.
1.4) Blood
A hematocrit should be checked post operatively for any patient who was dehydrated pre-operatively or who received large volumes during resuscitation and surgery, as well as for any who lost more than 75 cc of blood (less for children, according to size) prior to resuscitation-stabilization or intraoperatively. The timing and frequency of subsequent measurements should be guided by the initial post operative value and clinical picture.
Clotting parameters should be checked in patients with large amounts of intraoperative bleeding, those with known coagulopathy preop, those predisposed to developing coagulopathy (alcoholics, liver failure, leukemic, etc.) as well as those who received large volumes of blood products (especially when the products were not mixed with clotting factors - ie. Packed blood cells).
A white blood cell count should be measured post operatively in all patients in whom it was not measured preoperatively and then as indicated by fever, positive chest x-ray, and other clinical indicators of infection.
Electrolytes should be checked once post operatively and then as indicated clinically. In patients remaining intubated postoperatively a chest x-ray should be done postoperatively if not done pre-operatively, and for any patient with fevers or findings on chest auscultation, or with a known aspiration or suspicion thereof.
2. Neurologic
Neurologic monitoring during the intensive post operative care period requires integration of physical exam, intracranial pressure, and computerized tomographic data.
2.1) Exam
The clinical assessment of post operative brain function is based on the findings on neurological exam. Neurologic exams are essential for detection of post- operative neurologic deficits. Serial assessments of GCS and pupillary reactivity should be done hourly for the first four to six hours following return to the ICU and every four hours thereafter. Patients stable enough to no longer require neuro checks every four hours are ready for transfer to a lower acuity of care (neuro checks every 8 hours) unit.
a) Glascow Coma Score
The Glascow Coma Score should monitored serially at fixed intervals every hour from the time arrives back in the ICU or in recovery until the patient has emerged totally from anesthesia or at least to the point that an accurate Glascow Coma Score can be obtained. Once the patient is as awake as he or she will be the GCS should be taken at least once every two hours for the first eight postoperative hours, and then every four hours for the net sixteen postoperative hours such that the total time of frequent neurologic assessment is the first twenty four hours post op.
A lowering of the GCS by two or more points on the first post anesthetic neurologic assessment is an indication for re-scanning the patient.
b) Pupils
Pupils that preoperatively were equal that postoperatively are unequal should alert the surgeon to the possible of a re-bleed with more mass effect or evolution of cerebral edema with transtentorial herniation. Monitoring pupillary reactivity at regular intervals is a sensitive means for detecting herniation or rapidly rising intracranial pressure.
2.2) ICP
ICP monitoring should be continued post operatively in all patients with GCS of 8 or less preoperatively, patients with large subdural hematomas with GCS of 10 or less,
In the event that ICP monitoring is deferred to postop the procedure for insertion and maintenance of a monitor is described in the chapter on Optimization.
2.3) Cervical spine clearance
Cervical spine clearance is sometimes impossible prior to surgery in which case it becomes a priority of post operative monitoring and evaluation.
The optimum cervical spine clearance protocol remains controversial but probably will be based on the following principles: 1. in the presence of a mechanism of injury associated with a high incidence of cervical spine injury (whiplash, for example) every patient must be assumed to have an unstable cervical spine until proven otherwise. 2. passive dynamic testing in the comatose patient without normal self-protective cervical muscular mechanism and an unstable cervical spine can result in iatrogenic spinal cord injury. The consequence of principles 1 and 2 is that a large number of comatose patients with a possible accompanying cervical spine injury cannot be assessed by dynamic imaging necessary to be absolutely confident about the stability of the cervical spine. Fluoroscopy during passive flexion-extension for cervical spine dynamic imaging does not make the procedure much safer than would simply being careful and gentle when moving the potentially unstable cervical spine.
2.4) CT
To monitor for untoward evolution of intracranial pathology (such as rebleeding or declaration of stroke), CT scanning is indicated within 24 hours for every patient who after a head trauma craniotomy has a GCS of less than 14. Following this post op study, subsequent studies (in patients who do not require re-operation) are indicated only for a decrease in level of consciousness or appearance of a new focal deficit.
Immediate post op head CT is indicated for patients who fail to emerge from anesthesia within a time frame consistent with the drugs administered, where there is a new post operative neurologic deficit, or when the surgeon is concerned about post operative swelling due to the intraoperative condition of the brain, or about early recurrent clot due to his failure to obtain Grade One hemostasis prior to closure.
The three elements that must be accurately evaluated radiographically are clot, shift and infarction. The patient's preoperative CT is kept not only to justify the decision to operate but also to be compared to subsequent scans, in the immediate post operative period, and thereafter.
In general, if a patient is doing better than before surgery, there is no need to get a post op scan. In a patient who is doing better there is no justification, no matter how bad the lesion looks, to re-operate. Better not to scan than to find something that must be dealt with or if not, only with good justification to family, colleagues, and lawyer.
Head trauma post operative complications can be classified temporally as immediate or delayed, anatomically as intracranial, extracranial, or systemic, and etiologically as surgical, non-surgical post-traumatic, non-surgical iatrogenic, infectious, or physiologic.
TABLE: Head trauma craniotomy post op complications (intracranial)
| CLASSIFICATION SCHEME |
| Temporal |
| sdf |
Immediate |
rebleed |
| sdf |
Delayed |
rebleed |
| sdf |
Long term |
Chronic subdural, epilepsy, post concussive |
| Anatomic |
| sdf |
Intracranial |
sdf |
| sdf |
Extracranial |
sdf |
| Etiologic |
| sdf |
Neurologic non-surgical traumatic |
Malignant brain swelling, herniation, DIC |
| sdf |
Non-neurologic non-surgical traumatic |
sdf |
| sdf |
Surgical |
sdf |
| sdf |
Non-surgical iatrogenic |
sdf |
Immediate complications include re-accumulation of blood immediately or shortly after a surgical evacuation due to poor hemostasis at the time of closure. Whether from a persistent slow ooze or an errant inadequately coagulated arterial end, such hemorrhage is always avoidable with more time and attention spent intraoperatively to stopping all active bleeding.
Bleeding can be an immediate post operative event or occur in a delayed fashion. Any patient whose neurologic status deteriorates in the first few days post op should be suspected of harboring a recurrent or new hematoma. Even weeks or months after head injury, neurologic deterioration or headaches should be worked up for a chronic subdural hematoma.
Incisional bleeding beginning at the time of closure may manifest even prior to transfer to the ICU or not be detectable for more than 24 hours after operation. Fluid collections are frequent under the scalp flap due to tracking of blood and serum in the subgaleal space. These collections can track down between the fascial layers of the forehead and eyes to result in supraorbital ecchymosis and swelling of the lid sufficient that the eye is shut. The major problem with the eye swollen shut is that it the pupil behind the lid may be un-examinable until the swelling goes down.
Non-surgical post-traumatic complications include: Many of the complications following head trauma surgery are due to the patholphysiology of the head injury itself. These include malignant brain swelling (previously mentioned in the section on Intraoperative Problems), and herniation. Non-surgical iatrogenic complications: metabolic and respiratory alkalosis, hypokalemia, Infectious complications: extracranial of the wound, or intracranial of the brain or its coverings. Physiologic complications: GI bleeding, deep vein thrombosis with or without pulmonary embolism, decubitus pressure ulcerations, anemia.
1. Incisional bleeding
Post operative incisional bleeding is most likely due to inadequate hemostasis during scalp flap closure. That the blood vessels that bleed into the dressings the first few hours after a craniotomy are relatively close to the surface is proven by the effectiveness at preventing post operative inicisional bleeding of putting in two or three times the usual number of staples for each 10 centimeters of skin incision.
Incisional bleeding frequently will not stop with the relatively small amount of local tamponade one gets by changing the dressing and making it tighter. Head dressings that are made too tight risk other complications and are very uncomfortable for conscious or semiconscious patients. Sutures (000-nylon) placed along the skin incision line is usually effective in stopping post op incisional bleeding.
2. Elevated intracranial pressure
ICP elevation is a frequent accompaniment to severe head injury by whatever mechanism. High ICP is directly associated with increased intracranial resistance to intracranial entry and circulation of systolically pressurized oxygenated arterial blood Without perfusion, cerebral tissue dies by a number of mechanisms in which oygen, free radicals, excitotoxins, leukotrienes, and prostaglandins (not to mention nitric oxide, xanthine, VIP, and perhaps even melatonin) appear to play promient roles.
Detection of elevated ICP without an intracranial pressure monitor is very difficult in patients conscious or unconscious. In conscious patients ICP elevation can be asynptomatic or associated with relatively non-specific complaints such as "headache" or "dizziness". In comatose patients the GCS may not decrease inverse to elevation in ICP. The only way to detect ICP elevation is with an intracranial monitor.
Prevention --No known medication or therapy prevents ICP elevation better than any other.
Evaluation of elevated ICP - CT scan looking for evolution of cerebral edema, clot new or larger.
Management of elevated ICP is another area of continued controversy (in spite of, or because of, the recently issued Guidelines for the Management of Severe Head Injury,
3. Rebleed
Bleeding at a new level with respect to the layers of covering of the brain or with respect to brain regions can occur following otherwise uneventful removal of an intracranial hematoma. The new hematoma at a layer more or less superficial than that removed (i.e.: an epidural following removal of a subdural at the same location) is usually the result of inadequate hemostasis during closure. A left temporal subdural hematoma following evacuation of a right temporal epidural hematoma may form unexpectedly and unpredictably not as a clear consequence of surgeon inattention or error.
Presentation of rebleeds: with increase in ICP, with change in neurologic exam, detected on routine post op CT.
Detection of rebleeds: Even with an elevation in ICP and even with clear lateralizing signs (unilateral cycloplegia, hemiparesis) the location and size of a post operative rebleed cannot be determined with a fraction of the certainty possible with computerized tomography.
The surgical management of a rebleed is complicated by considerations of the patient's pre- and post-operative neurologic status. A patient with a GCS of 4 or 5 pre op and 12 hours post craniotomy for hematoma evacuation is less likely to return to the OR if his routine post op scan shows a recurrence of his 2 cm subdural hematoma than a patient with a GCS of 14 or 15 pre op with a GCS 4 or 5 12 hours post craniotomy for a contralateral t frontotemporal epidural hematoma seen
3.1) Recurrent hematoma (same site)
Prevention: prevention of recurrent hematoma requires good hemostasis at the time of closure.
A recurrent clot can be due to inadequate hemostasis at the time of closure but can also result from bleeding diathesis due to clotting factor depletion or deficiency or from hypertension. These factors is present may contribute to a post op clot due to inadequate closure hemostasis.
Prevention of recurrent clot formation depends on the mechanism of clot formation in the first place. Anesthesia control of blood pressure.
Check clotting factors post op and next day.
An intraparenchymal clot will reaccumulate unless the oozing from small blood vessels in the parenchymal tract has been stopped of course, but also if the means of controlling bleeding from a larger source is inadequate or tenuous.
Any post operative neurologic deterioration without a clearly identifiable extracranial cause requires an emergency head scan.
Clinically significant hematomas should be evacuated.
3.2) New intracranial hematoma (new site)
New clots post op at sites removed from the surgical site are usually due to alterations in the pressure dynamics or shifts among the intracranial contents.
Contralateral extra-axial hematoma formation is not infrequent after evacuation of a large subdural or epidural hematoma.
Hemorrhage at pre-operatively uninvolved sites can be prevented by minimizing shifts in the position of the brain within the cranium. Such acceleration-deceleration shifts are associated with tearing of bridging veins and formation of subdural hematoma.
The management of a new post operative clot begins with a suspicion for such in the patient with a deterioration in neurologic status post op, or failure to wake up. Identification with imaging.
Monitoring both clinical and, iicaf indted, by intracranial pressure monitoring.
If the bleeding persists the patient will develop a potentially life-threatening subdural or subarachnoid clot. Open the dura is suspicious that this is the case.
Injury to the surface of the brain can be problematic if it is associated with laceration of pial vessels. This can occur during placing of dural tenting sutures or when an instrument inadvertently touches the brain surface.
Occult bleeding is from vessels that cannot be directly visualized because of their small calibre or location under a bone flap edge (or other visually obstructing structure). These vessels are large enough to be tamponaded or coagulated but must first be identified.
Subdural hematomas are notorious for being due to vessels large enough to cause annoying intraoperative and potentially postoperative bleeding but so small as to be elusive of visual identification and localization. What surgeon has not had the sudden realization that minutes or hours of chasing occult venous bleeders and not the anticipated closure usually follow lifting off of subdural clot.
The surest way to find and dispatch errant occult bleeders is to be familiar with their anatomy. Bridging veins are not located over the entire surface of the brain, but rather toward the midline near the vertex traversed by the sagittal sinus into which they must all drain (that's the space - cortical surface to dural sinus wall - "bridged" by bridging veins!). The bleeding after a subdural is lifted off the surface of the brain is most likely from bridging veins. Look for them, as their anatomy would suggest, near the midline, along the vertex.
Epidural hematomas form from a laceration of the middle meningeal artery anywhere along its dural course. From its entry through the foramen spinosum into the cranium, the middle meningeal artery lies on the floor of the temporal fossa, inaccessible to the surgeon except with temporal lobe retraction. Such retraction may be necessary to identify and stop middle meningeal bleeding but can be minimized by familiarity with the dural course of the middle meningeal artery. If necessary examination of its entire intracranial dural course, the artery can be safely exposed in two or three minutes.
Above are strategies for visualizing the sites of initially occult bleeding. Sometimes there is no strategy that works. Frequently from under an overhang of bone there is epidural, subdural, or subarachnoid bleeding. This bleeding is most often supposed to be and probably is subdural but epidural and subarachnoid bleeding into the operative field from under a bone flap are possible as well.
Stopping occult bleeding from an unknown source is difficult because measures taken to stop bleeding from one layer or locating may provoke it at another. Surgicel gently tucked into the epidural space along a bone edge is an effective physical barrier to blood running out onto the dura from under the bone. As long as it is not under pressure, the epidural blood will accumulate only until the epidural mass pressure equals and then exceeds that within the lumina of the epidural vessels. A common mistake is to overestimate the amount of pressure or mass required stopping epidural bone edge bleeding. There is need neither for large amounts or impacting forces. The larger the mass, the greater the force, the more likely is further dissection of dural from the cranium with consequent small vessel bleeding and clot formation - all within a space covered from the surgeon's vision by bone.
DIC is associated intraoperatively with a generalized ooze. Postoperatively it may be associated with postoperative bleeding into either the site of a recent hematoma evacuation or a new intra- or extra-axial site.
Even though not due to the disruption of blood vessels. Control of disseminated intravascular coagulation is the responsibility of the surgeon.
3.3) Iatrogenic subdural hematoma mechanism
When doing decompressive surgery, either removing brain tissue or large intracerebral hematomas, it is possible to rapidly increase the distance between the cortical surface and their sagittal sinus across which are stretched the bridging veins. These can tear, resulting in subdural hematoma. Watch for bleeding from the bridging veins if possible and try not to manipulate the brain such that is tends to put tearing forces on them. Very old patients may have extremely friable skin. Laceration of this can be avoided by too much pulling, placement of the pins so that they do not move. This skill will also tend to bruise easily. Thus it is advisable to avoid any percussive forces.
II. Extended acute (36 hours to 10 days)
1. Infection
Infections are frequent in the neurosurgical ICU. Usually these are with common organisms that still are susceptible to relatively cheap and readily available antibiotics. In addition to the causes of post op infection (pneumonia, urinary tract infection, etc.) certain infections are more frequently seen in head trauma craniotomy patients.
Steroids contribute to a higher incidence of infection especially after two to three weeks' administration.
Post op infection is prevented by appropriate sterile technique during dressing changes and attention to patient hygiene. Perioperative antibiotics should be discontinued 24 to 48 hours post operatively.
Post operative infections are worked up as any infection: Chest Xray, urine, sputum, blood, spinal flood cultures, white count and differential, ESR.
Post operative infection is managed according to standard principles of antibiotic selection, dosage, and administration. Patients with infected ventriculostomies require removal of the infected apparatus with placement at a virgin contralateral site.
Intracranial and extracranial infection post head trauma surgery are frequently delayed in part because the pathogens tend to be normal flora of the skin.
A wound infection can be manifest as early as two days post op. Typically it presents as warmth, redness, and swelling along the incision. There may be an associated fever and elevation of the white blood cell count, but "calor, rubor, and dolor" are more compelling than changes in temperature or CBC in making the diagnosis of wound infection.
Infection can exacerbate facial swelling by stimulating purulent effusions into the subgaleal space. A serosanguinous fluid collection is a favorable culture media for bacteria. Fluid collections associated with warmth and erythema (redness) of the overlying scalp should be tapped by placing a large bore spinal needle directly through the skin and scalp into the collection at its thickest point. As must fluid as possible should be drawn out and sent for microbiologic analysis. Broad spectrum antibiotics started immediately after such a tap can be changed if once sensitivities are known for infecting organisms or stopped if infection is absent on final culture result.
The surgeon must assume that the devitalized bone flap under an infected subgaleal fluid collection harbors pathogenic organisms as well. The bone flap must in this circumstance be removed. Cranioplasty to cover the resulting cranial defect should be done no less than six months after the wound-bone flap infection has been treated and cleared.
Brain abscess can be an indolent infection with no harbinger temperature, blood count, or even neurologic changes. Suspicion of brain abscess should be high for all penetrating missile injuries and open depressed skull fractures associated with parenchymal contamination. Bacterial meningitis post head trauma surgery is a more fulminant infection with a more dramatic presentation usually with mental status changes, fever, and neck stiffness.
2. CSF leak
CSF leaks extracranially when three conditions obtain: 1. Incompetence of the dura mater 2. Defect of skull 3. Lower pressure extra- than intracranial. A CSF leak stops when any or all of these conditions are eliminated. The third, namely the extra-intracranial pressure gradient, is the only condition that can be treated without bringing the patient back to the OR. The downward intracranial to extracranial gradient can be neutralized or reversed by: raising the head of the bed, removing CSF (ventricular catheter, lumbar drain, lumbar puncture), or decreasing intracranial pressure. If prayer works it is probably because assisted by unseen shifts in tissue (brain or blood clot) which occlude holes in the dura or skull. Fortunately prayer and head elevation work in the majority of post traumatic (non-penetrating) CSF leaks.
Deep vein thrombus formation and propagation is a concern in patients who are not spontaneously moving their lower extremities.
3. Deep vein thrombosis
3.1) Presentation and detection
In the conscious patient, history of pain in the calves (associated with a positive Holman's maneuver) is virtually diagnostic of a DVT. In the comatose patient the diagnosis depends more on the results of VQ scanning and other pulmonary function tests.
3.2) Evaluation
Deep vein thrombosis is evaluated by a number of tests that can be done immediately after a head trauma craniotomy.
3.3) Causes
Venous stasis due to patient immobility.
3.4) Management
Compression stockings (passive or dynamic ), anticoagulation (heparin - no sooner than 24 hours following craniotomy for hematoma evacuation), and inferior vena cava filter are the primarily means used to prevent DVT.
3.5) Prevention
Deep vein thrombosis in the post operative period can be controlled by mechanical and pharmacologic means. Leg squeezers. Subcutaneous heparin. Inferior vena cava filter. Early mobilization.
Management of deep vein thrombosis
4. GI bleeding
The causes of post operative GI bleeding include use of steroids as well as a stress response to the head injury.
Some GI bleeding can be prevented by starting to use the gut as early as possible. Tube feedings
Management of post op GI bleeding
5. Anemia
The brain's high demand for oxygen makes anemia with compromise of oxygen delivery, potentially damaging to nervous tissue.
Causes of post op anemia
Pre-op bleeding. Scalp lacerations. Intra-operative bleeding.
Prevention of post op anemia
Suture wounds in ER. Hemostatic techniques. Prevent coagulopathy.
Management of post op anemia
Transfusion to keep Hct above 25.
6. Skin breakdown
Causes of skin breakdown
Areas of skin breakdown due to prolonged pressure and resultant ischemia occur in the immobilized (paralyzed) patient at sites where extremities make contact with unyielding surfaces on the operative table…
Prevention of skin breakdown
Pressure sores can be prevented by identification and padding of sites of thin soft tissue between bone and OR table surface.
Management of skin breakdown
Depends on the severity of the injury. Stages of decubiti and all that… One thing the surgeon can do is to order a softer bed.
7. Seizure
7.1) Causes
Any source of cortical irritation, whether pre- or post-traumatic will be more likely to incite seizures (so-called "epileptogenic") in the presence of focal metabolic and electrolyte imbalance frequent after severe head injury.
The surgeon must assume that every post operative seizure is a surgical complication until proven otherwise. Every post op seizure is due to a space occupying intra- or extra-axial hematoma until these have been radiographically ruled out.
7.2) Prevention
A chemically and electrically homeostatic environment is least favorable to the initiation and propagation of seizure activity. The same space occupying cortical irritant lesion incites synchronous electrical activity sooner among populations of neurons vulnerable due to intra- and extra-cellular metabolic imbalance. Maintain electrolytes, especially sodium, as close to normal levels as possible. Watch for and treat the syndrome of inappropriate antidiuretic hormone (SIADH).
The resistance of a metabolically normalized neural environment to seizures is enhanced by membrane-stabilizing anticonvulsant drugs. Any patient, surgical or not, who has suffered a severe head injury is a candidate for seizure prophylactic medications. The trauma to the cortex of removing a subdural or intraparenchymal hematoma can be yet another provocation to seizure and is an indication for post operative anticonvulsants.
Foreign bodies in contact with electrically active cells act as foci of irritation and are believed to be associated with seizure activity in a many traumatic and non-traumatic neurosurgical scenarios. The argument against intraparenchymal, subarachnoid, or subdural drains post op is not only infection risk, but that of seizure as well.
7.3) Management
The problematic aspect of post operative seizure management for most head trauma surgeons is not in the selection or dosing of an appropriate anticonvulsant, but of the appropriate circumstance for institution of long term anticonvulsant therapy. Recent reports of a very low incidence of seizures among large and pathologically diverse populations of head trauma victims do not argue against the concept of preventing this dangerous short and long term potentially recurrent post traumatic condition but suggest that the incidence of post-traumatic epilepsy is much lower than previously believed.
Even when decision has been made to put the patient on post operative anticonvulsants, when the appropriate dose for the patient weight has been accurately calculated, and the drug carefully prepared and administered, the post op head trauma patient can STILL have a seizure.
Management of a post op seizure requires simultaneous diagnostic and therapeutic measures. Three diagnostic considerations have been discussed and must each be ruled out: the metabolic environment, the presence of therapeutic levels of anticonvulsant drugs, and any space occupying, potentially epileptogenic, mass lesion.
7.4) Prevention
A chemically and electrically homeostatic environment is least favorable to the initiation and propagation of seizure activity. The same space occupying cortical irritant lesion incites synchronous electrical activity sooner among populations of neurons vulnerable due to intra- and extra-cellular metabolic imbalance. Maintain electrolytes, especially sodium, as close to normal levels as possible. Watch for and treat the syndrome of inappropriate antidiuretic hormone (SIADH).
The resistance of a metabolically normalized neural environment to seizures is enhanced by membrane-stabilizing anticonvulsant drugs. Any patient, surgical or not, who has suffered a severe head injury is a candidate for seizure prophylactic medications. The trauma to the cortex of removing a subdural or intraparenchymal hematoma can be yet another provocation to seizure and is an indication for post operative anticonvulsants.
Foreign bodies in contact with electrically active cells act as foci of irritation and are believed to be associated with seizure activity in a many traumatic and non-traumatic neurosurgical scenarios. The argument against intraparenchymal, subarachnoid, or subdural drains post op is not only infection risk, but that of seizure as well.
III. Subacute (10 days to 2 months)
IV. Permanent (more than 2 months)
The head trauma surgeon will find himself involved in the long term care particularly of those who do well enough post operatively to leave the hospital conscious and not in need of acute medical care. Long term post op problems in good outcome patients are seen in the ambulatory care clinic. Sometimes the surgeon will have to make a determination of the patient's fitness for his usual or any employment, frequently he will be asked to decide when a patient is ready to begin driving again, and he should always be ready to make suitable referrals for social worker, psychiatrist, or other non-surgical medical interventions.
The head trauma surgeon should not manage long term anticonvulsant administration deferring complicated issues of seizure control to colleagues in neurology. Anticonvulsants are probably indicated for six months after head injury associated with cortical violation (such as contusion, depressed skull fracture with parenchymal involvement, and penetrating missile injuries) as well as subdural hematomas requiring surgical evacuation. The complexity of the issue in terms of implications for driving and employment, combined with the ambiguity in the clinical neuroscientific literature justifies the head trauma surgeon in seeking neurological consultation regarding long term anticonvulsant management.
Although seldom indicated later than two weeks post injury, follow up imaging weeks, months, even years after a head injury operation may sometimes provide important diagnostic and prognostic information.
Changes on CT that can evolve over time and not be manifest on studies done while in the hospital or in the acute post operative care period include definition of areas of encephalomalacia around intracerebral hematomas and contusions, declaration and maturation of areas that have suffered ischemia, and development of infections of the CSF spaces or brain parenchyma.
Rehabilitation is supervised by a team of mental health, medical, and social workers who invoke the head trauma surgeon only in the event that the patient develops a complaint potentially referable to his surgery or fails to progress in his rehabilitation program.
A small but gratifying number of patients who come in with low Glascow Coma Scale scores and other indicators suggestive of poor prognosis for post-operative neurologic recovery wake up long after the onset of coma. If the head trauma surgeon is the primary person following a head trauma victim long term because the neurologic status is too poor to justify rehabilitation or therapy, he should be aware of the signs of delayed emergence from coma into a state receptive to therapies and rehabilitation.
Some patients are concerned about the hole in their head left when the bone flap was left out at the time of the first surgical intervention. As discussed above, the fact that routinely leaving out the bone flap should be condemned, does not mean that there are not situations where the surgeon leaves out the bone flap due to legitimate pathophysiologic considerations.
A surprising number of patients who were snatched from the jaws of death are not grateful to their rescuer but rather criticize him for a scar that is itchy, red, or tender. With more justification they may complain that the scar is too far in front of the hairline.
Skull defects after head trauma surgery result from extensive craniectomies or from elevation of depressed skull fractures where not all of the cranial fragments can be replaced, as well as from craniotomies (hopefully infrequent) where the surgeon decided to leave the bone flap out at closure. Not all defects need to be covered.
Safety is a more compelling indication for cranioplasty than cosmesis. Large suboccipital defects are not unsafe because they are covered by several thick layers of cervical muscle. Defects of the temporal region just above the zygoma are usually covered by enough temporalis muscle that the patient is not at undue risk from blunt focal impacts there. Defects over the calvarium leave the underlying brain covered only by the scalp and should probably be covered if they are greater than 7 or 8 centimeters in their smallest dimension. The head trauma surgeon should be sympathetic to requests for cosmetic cranioplasty for disfiguring defects in areas not covered by hair.
Cranioplasty can be done within three months of head trauma craniotomy if the bone was left out at the initial surgery in the absence of infection. As noted above, cranioplasty must be delayed at least six months if the bone flap removal was associated with primary or contiguous infection. The cranioplasty procedure is described in the chapter on generic craniotomy techniques.
POSTOPERATIVE COMPLICATIONS
Post operative complications can be separated into those which are neurological and those which are not. Non-neurological complications include: infection extracranial of the wound, or intracranial of the brain or its coverings, gastrointestinal bleeding, anemia, formation of deep vein thrombosis (with or without pulmonary embolism), and development of pressure sores of the skin.
Non neurological
Infection (with or without sepsis)
Causes
Use of steroids
Prevention
Prevention of post operative infection … perioperative antibiotics
Management
Post operative infection is managed ..
Pneumonia
Causes
Post operative pneumonia is a frequent complication of head trauma surgery.
Prevention
Prevention of post operative pneumonia
Management
Post operative pneumonia is managed by…
GI bleeding
Causes
The causes of post operative GI bleeding include use of steroids as well as a stress response to the head injury.
Use of steroids
Prevention
Some GI bleeding can be prevented by starting to use the gut as early as possible. Tube feedings
Management
Anemia
The brain's high demand for oxygen makes anemia with compromise of oxygen delivery, potentially damaging to nervous tissue.
Causes
Pre-op bleeding. Scalp lacerations. Intra-operative bleeding.
Prevention
Suture wounds in ER. Hemostatic techniques. Prevent coagulopathy.
Management
Transfusion to keep Hct above 25.
Deep vein thrombosis
Causes
Venous stasis due to patient immobility/
Prevention
Leg squeezers. Subcutaneous heparin. Inferior vena cava filter. Early mobilization.
Management
Skin breakdown
Causes
Areas of skin breakdown due to prolonged pressure and resultant ischemia occur in the immobilized (paralyzed) patient at sites where extremities make contact with unyielding surfaces on the operative table…
Prevention
Pressure sores can be prevented by identification and padding of sites of thin soft tissue between bone and OR table surface.
Management
Depends on the severity of the injury. Stages of decubiti and all that… One thing the surgeon can do is to order a softer bed.
Neurological
Intracranial hematoma
Recurrent
Causes
A recurrent clot can be due to inadequate hemostasis at the time of closure but can also result from bleeding diathesis due to clotting factor depletion or deficiency or from hypertension. These factors is present may contribute to a post op clot due to inadequate closure hemostasis.
Prevention
Prevention of recurrent clot formation depends on the mechanism of clot formation in the first place. Anesthesia control of blood pressure.
Check clotting factors post op and next day.
An intraparenchymal clot will reaccumulate unless the oozing from small blood vessels in the parenchymal tract has been stopped of course, but also if the means of controlling bleeding from a larger source is inadequate or tenuous.
Management
Identification of the presence of a recurrent clot precedes attempts at management.
Any post operative neurologic deterioration without a clearly identifiable extracranial cause requires an emergency head scan.
New Intracranial Hematoma
Causes
New clots post op at sites removed from the surgical site are usually due to alterations in the pressure dynamics or shifts among the intracranial contents.
Contralateral extra-axial hematoma formation is not infrequent after evacuation of a large subdural or epidural hematoma.
Prevention
Hemorrhage at pre-operatively uninvolved sites can be prevented by minimizing shifts in the position of the brain within the cranium. Such acceleration-deceleration shifts are associated with tearing of bridging veins and formation of subdural hematoma.
Management
The management of a new post operative clot begins with a suspicion for such in the patient with a deterioration in neurologic status post op, or failure to wake up. Identification with imaging.
Monitoring both clinical and, if indicated, by intracranial pressure monitoring.
I. Physiologic
Precipitous changes in the patient’s hemodynamic status such as hypotension, arrhythmia, and oxygen are intraoperative crises that can sabotage an otherwise successful head trauma operation.
The anesthesiologist should be competent at managing heart rate, ventilation, and other physiologic crises without interfering with what the surgeon is trying to do. The surgeon must be ready to modify (usually shorten) surgery if anesthesia is unable to correct key physiologic parameters.
Some of the shortcuts described in the chapter on Planning, such as leaving the dura open, not replacing the bone flap, or deferring ventriculostomy placement to post op may be appropriate or even necessary in the face of an intraoperative physiologic crisis.
If abnormalities of vital signs are severe, resistant to prompt resuscitation, or responsive only transiently even after multiple resuscitations attempts, surgery, with the assent and cooperation of anesthesia, should be aborted and the patient transferred to the Intensive Care Unit forthwith.
To prevent intraoperative physiologic crises try to keep the patient’s physiologic parameters normalized as much as possible. Stop active extracranial bleeding from the face and scalp.
Before reacting to a change in vital signs, make sure that the change is real. Verify that the monitoring devices indicating an abnormality are fully functional. Changes in ventilation are frequently not physiologic but mechanical – slippage of the endotracheal tube or someone carelessly leaning on and compressing it, the most common causes. The O2 monitor may have slipped off the patient’s earlobe or finger.
Physiologic monitoring has great value in the treatment as well as detection of physiologic crises. Volume status is assessed by central venous pressure monitoring, collection and measurement of urine output. Cardiac output and systemic vascular resistance are parameters derived from thermodilution-capable catheters such as the Swan Ganz but are superfluous in the setting of head trauma operations. End tidal CO2 and arterial O2 reflect ventilation and oxygenation respectively. An arterial line or automatic blood pressure cuff monitor blood pressure.
A. Hypoperfusion (hemodynamic collapse)
Intraoperative detection and management of hypoperfusion is a joint anesthesiology and neurosurgery responsibility.
1. Manifestation
Hypotension and tachycardia are the vital signs abnormalities associated with hypoperfusion. Urine output decreases. The blood gas shows acidosis. If measured, lactate is elevated. Arrhythmias associated with acidosis are sometimes detected on EKG.
2. Etiology
Treatment of hypotension requires knowledge of and familiarity with the medical management of the most commonly invoked patho-etiologic factors.
3. Management
Hypoperfusion should be treated aggressively to maintain substrate delivery and cellular function of the vital organs (including the brain). Exacerbation of cerebral edema is a theortetical concern but not enough of one clinically to withhold fluid for systemic, cardiac, and cerebral perfusion to keep the patient’s brain “dry”.
Hypotension should be managed with pressor support if hydration does not raise mean arterial pressure.
4. Avoidance
Head trauma craniotomies are frequently done on patients with trauma to other organs and extremities causing systemic hypoperfusion secondarily impacting on that of the brain. Avoidance of hemodynamic collapse requires maintenance adequate volume and blood pressure.
B. Hypovolemia
1. Recognition
2. Etiology
3. Management
Management of hypovolemia includes administration (with supplementation as necessary) of oxygen directly into the patient’s respiratory tract.
Volume should be restored by a combination of colloid and crystalloid titrated to urine output, blood pressure, central venous pressure and cardiac output (if available) as well as hematocrit, BUN and creatinine, and electrolytes (especially soldium).
Pressors may be required transiently to maintain perfusion in hypovolemic patients but can usually be discontinued once the patient is rehydrated.
Efforts should be made to identify and stop any bleeding that could be contributing to hypovolemia. Slow but diffuse bleeding from a long scalp incision can result in lowering of the hematocrit and oxygen carrying capacity of the blood.
Management of intraoperative physiologic crises begins with a determination of the causes. Increased intracranial pressure causes the Cushing response -- a triad of bradycardia, hypertension, and respiratory abnormalities. Overzealous diuresis to reduce intracranial pressure control (especially without attention to volume status) can result in hypotension with compromise of cerebral perfusion and exacerbation of tachyarrhythmias.
Hypovolemic hypotension (frequently secondary to aggressive diuresis, treated with iso- or hypertonic fluid or whole blood or, if these fail with catecholamine pressor drips. Success of treatment is reflected in decrease of heart rate towards normal, increase in mean arterial pressure and urine output, and, most important (here another argument for preoperative placement of intracranial pressure monitoring devices) in normalization of cerebral perfusion pressure.
In extreme cases where ongoing hemorrhage cannot be controlled it may be necessary to temporarily stop the procedure.
4. Stop procedure
C. Monitoring
D. Blood products
E. Hemostasis
1. Shorten procedure
Hypoperfusion shock frequently confounds interpretation of hemodynamic parameters. Idiosyncratic reactions to anesthetic or other pharmacologic agents administered pre- and post-operatively (such as Dilantin or a beta-lactam antibiotic) can provoke physiologic parameter measurements identical those of sepsis or shock. In addition to those of the Cushing Response, other neurogenic vital sign crises include those of arrhythmia and oxygen desaturation (neurogenic pulmonary edema)
2. Avoidance
F. Hypoxia
Hypoxia is condition of tissue oxygen deprivation resulting (in the discussion that follows) from inadequate blood oxygen supply.
1. Recognition
One of the most common manifestations of hypoxia, namely, cerebral cortical dysfunction (clinically: mental status alteratio)n, is detectable in the comatose patient only by electrophysiologic testing (ie. EEG)
The other common and most life threatening complication of hypoxia is myocardial infarction. The added stress of a head injury subjects the heart to increased oxygen demand. Myocardial infarction occurs when the cardiac blood delivey capacity(hypovolemia) or oxygen carrying capacity (anemia) decrease.
2. Etiology
The most common etiology of intraoperative hypoxia is
3. Management
Hypoxia
4. Avoidance
Avoidance of hypoxia
G. Air embolism
1. Recognition