Hospital Practice

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Effective Management of Penetrating Head Injury Michael J. Lacqua & Pradip Sahdev To cite this article: Michael J. Lacqua & Pradip Sahdev (1992) Effective Management of Penetrating Head Injury, Hospital Practice, 27:9, 30-50, DOI: 10.1080/21548331.1992.11705480 To link to this article: http://dx.doi.org/10.1080/21548331.1992.11705480

Published online: 17 May 2016.

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Date: 13 June 2016, At: 17:47

Clinical Review

Effective Management of Penetrating Head InjuryMICHAEL J. LAC QUA and PRADIP SAHDEV

Nassau County Medical Center, East Meadow, N.Y.

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Although head injuries are usually easily recognized, other, less obvious lesions should also be promptly investigated. In either case, outcome is often determined in the first few minutes and hours of management. An estimated 410,000 persons

sustain head injuries annually in the United States; 300,000 of them require hospital admission. Nearly 18,000 patients are left with moderate to severe neurologic deficits, and 2,000 remain in a vegetative state. Although the number of penetrating injuries occurring nationwide is unknown, a recent review of 16,524 head injuries treated at 95 trauma centers over a fouryear period reported that 4.6% of the injuries were caused by firearms and 0.4% were stab wounds (Table 1). Because of the brain's vulnerability to irreversible damage, early and aggressive management of penetrating head injuries must begin with the primary care provider. Effective pei'formance of this task rests on an understanding of the anatomy and physiology of the brain. In the human adult, the skull encloses a space about 1,500 cc in volume. More than 90% of this space is occupied by the brain, and the rest by cerebrospinal fluid. Because of the rigid construction of the skull, bleeding into this space will cause a rapid increase in pressure, with consequent compression of the brain. 30

Hospital Practice September 15. 1992

Thus, in sharp contrast to the other two body cavities, the abdomen and the chest-each of which can sequester several liters of blood-the skull cannot accommodate hemorrhage exceeding a few hundred cubic centimeters. Pressure on the brain must be relieved quickly by surgical evacuation of the blood clot (if one is present) or by reducing brain edema by medical means. Since hemodynamic instability in the vast majority of trauma patients results from blood loss, head injury alone must not be held responsible for traumatic shock; a source of hemorrhage must be searched for and treated. An essential concept in the understanding of head injury is the cerebral perfusion pressure (CPP)-the net pressure that results in perfusion of the brain. The CPP is defined as the mean arterial pressure (MAP) minus the intracranial pressure (ICP). In the normal state, the MAP is approximately 90 mm Hg and the ICP is about 10 mm Hg. Hence, the CPP is generally around 80 mm Hg. with a range between 50 and 150. If the arterial blood pressure falls or the intracranial pressure rises, the

CPP will fall. Once it falls to less than 30 mm Hg, cerebral perfusion stops and brain death occurs. The brain region injured has a major effect on the sequelae of severe trauma. The components of each of the three anatomic regions and their physiologic functions are summarized in Table 2. The midbrain and hindbrain maintain vital functions. If they are intact, a patient may survive in a vegetative state when functions that reside in the forebrain (e.g., personality, memory, intelligence) have been lost. In contrast, injury localized to the hindbrain may result in early death, because regulation of vital functions such as respiration and blood pressure is imperiled.

Diagnosis In most cases, penetrating injury to the head is easily recognized. A history of firearm or stab wounds, together with the appearance of a head wound and altered mental state, leave little doubt as to the nature of the injury. On the other hand, it is imperative to evaluate the patient for additional injuries, even when just a head wound is ap-

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parent. This includes not only evaluation of adjacent areas (face, oropharynx, and neck) for involvement but also examination for unsuspected body wounds. Wounds of the face and upper neck, especially those caused by firearms, may involve the intracranial structures directly, by penetrating the skull, or indirectly, by interrupting blood supply to the brain. In one series, 20 of 38 patients with penetrating trauma of the forehead also had intracranial penetration. Additionally, eight of 24 patients with penetrating injury to the mid-face had involvement of the orbital contents. Penetrating neck trauma may cause injury to the carotid artery, with disruption of the blood supply to the brain and resultant neurologic deficits. Injury to either the face or the neck should therefore alert medical personnel to perform a rapid but thorough neurologic examination. Some additional signs should be noted in patients with known or suspected head injury: Raccoon's eyes. Discoloration or bruising around one or both eyes (Figure 1) indicates a fracture of the anterior skull base (anterior cranial fossa). CSF rhinorrhea. Leakage of cerebrospinal fluid from the nares signifies a basilar skull fracture, specifically in the region of the ethmoid sinuses. Hematympanum. Blood behind the eardrum signifies a fracture of the skull base in the midregion (the middle cranial fossa). Leakage of cerebrospinal fluid from the ear canal (CSF otorrhea) also signifies a fracture in the mid-skull base.

Table 1. Causes of Head Injury in 16,524 Patients• Mechanism

Percent

Enclosed motor vehicle accident

45.5

Nonpedestrian fall

15.0

Assault

13.7

Pedestrian accident

11.3

Motorcycle accident

9.5

Gunshot wound

4.6

Stab wound

0.4

*Adapted from Gennarelli TA et al, 1989

Battle sign. Discoloration behind the ear over the mastoid process signifies fracture of the posterior skull base (the posterior cranial fossa). It is important to appreciate that apparently minimal penetrating wounds to the head may

conceal dramatic features. Figure 2 is an example. With an entire knife blade embedded in her brain, the patient survived, because the blade penetrated the frontal lobe and caused relatively localized damage. Gunshot wounds, on the other hand, will often lead to major parenchymal

Table 2. Anatomic Regions and Physiologic Functions of the Human Brain Forebrain Cerebral hemispheres (including cerebral cortex) Hypothalamus

Highest levels of somatic control; responsible for memory, association, personality

--------------------------Integration of autonomic and endocrine mechanisms

Midbrain Tegmentum, corpora quadrigemia

Contains nuclei for control of eye movements, ocular and postural reflexes, nuclei for many visceral activities, and motor nuclei of cranial nerves Ill and IV

Hindbrain Medulla

Pons Cerebellum

Location of control of many vital functions; contains nuclei for many cranial nerves Contains fiber tracts and acts as relay

_~~~~n- ~o-~i~~:_r_c:~~e!~ ________ _ Helps maintain equilibrium and orientation in space; assists in maintaining muscle tone and coordination

Hospital Practice September 15. 1992

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Figure 1. In a patient with a self-inflicted gunshot wound to the right temple, the entry site was readily apparent. Discoloration around the Ipsilateral eye was indicative of anterior basal skull fracture resulting from the wound.

injury extending far beyond the actual path of the missile. Finally, any patient with a penetrating wound anywhere on the body who presents with altered mental state must be evaluated for an additional injury to the head. Some entrance wounds may be strategically concealed, making discovery difficult unless the wounds are sought diligently-for example, intraorally or under the scalp hair.

Immediate Management For patients with penetrating head injuries, just as for any trauma patient, evaluation and management . of the airway, breathing, and circulation must be performed first, followed by a survey and treatment of any injuries that may require urgent attention. However, there are some aspects of management that are relevant to the head-injury patient in particular. In the absence of associated facial or neck injuries, the patient's airway can usually be cleared by suctioning before placement of a nasal or oral tube. Unless the patient is awake and 32

fully responsive, early nasotracheal or orotracheal intubation should be undertaken to prevent aspiration and to permit hyperventilation. The possibility of cervical spine injury should be borne in mind, and the spine should be immobilized before any manipulations. Hyperventilation to decrease circulating carbon dioxide to between 28 and 32 mm Hg should be routine in any head-injury patient with significant neurologic compromise. Indeed, hyperventilation is probably the most effective initial maneuver to minimize brain edema and prevent brain herniation. All head-injury patients should be given 100% oxygen to maximize oxygen delivery to the brain. Availability of a portable pulse oximeter to measure blood oxygen saturation is ideal. As noted, hemodynamic instability in a head-injury patient is nearly always related to associated injuries. When identified, they must be treated, and concurrent shock should be addressed vigorously. Because scalp lacerations can cause enough blood loss to trigger

Hospital Practice September 15, 1992

shock, tamponade should be applied early. In the absence of associated injuries, loss ofvasomotor tone resulting in hypotension is often preterminal. It may be preceded by the Cushing reflex (hypertension and bradycardia). and, in the presence of dilated pupils, it signifies brain herniation. If there is no associated blood loss, crystalloids and blood should be administered judiciously, because overhydration will increase brain swelling and thus can worsen the ultimate prognosis. Hypotension, however, will decrease cerebral blood flow, and therefore may also cause cellular dysfunction or death. Careful titration of fluids to maintain systolic pressure above 90 mm Hg is essential. Measurement of central venous pressure through a central venous catheter is ideal, but may be difficult to do. The CVP should be maintained between 3 and 8 mm Hg. Pressure-stabilizing techniques may be particularly useful in inter hospital transfers. Military antishock trousers, though not contraindicated in penetrating head injury, provide no proven benefit. In fact, a widely cited study by K. L. Mattox and co-authors showed no survival advantage associated with prehospital use of the devices in head-injury patients. If they are used in cases of severe head injury, caution should be exercised. Medications have some role in the acute management of the head-injury patient. Mannitol and furosemide can help decrease cerebral edema temporarily, but their use is contraindicated in hemodynamically unstable patients. Pressors such as dopamine may be useful in cases of hypotension refractory to fluid replacement but are rarely indi(cont!nues)

HEAD INJURY

(conttnued}

cated early in treatment. Seizures, either focal or diffuse, must be controlled with diazepam, phenytoin, or other anticonvulsant medications. Other pharmacologic agents may be needed to paralyze an otherwise uncontrollable patient. Since the clinical examination is no longer reliable after the patient is paralyzed, this treatment should be avoided if at all possible.

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Definitive Care

Figure 2. Only a small scalp laceration was detected on physical examination. Skull x-rays in the anteroposterior (top) and lateral (bottom) views, however, showed that an entire knife blade was embedded in the brain.

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Hospital Practice September 15. 1992

Once the patient reaches the emergency department, the airway, breathing, and circulation need to be reassessed, and alterations in management made as indicated. A secondary survey and repeat neurologic examination is then performed. Rapid worsening of neurologic status indicates the presence of an expanding intracranial hematoma, which may respond to surgical drainage. If they have not already been done, endotracheal intubation and hyperventilation should be initiated. Nasagastric intubation for gastric decompression and Foley catheter drainage of the urinary bladder are also performed. A central line is placed percutaneously via the subclavian vein to measure central venous pressure and provide vascular access. X-rays of the skull, face, cervical ~pine, and chest are performed, followed by a CT scan of the head. Further treatment is governed by the patient's clinical status and the tomographic findings. When a localized foreign body is found (see Figure 2), emergency craniotomy and removal of the object may be indicated (as was done in that patient). In other cases, involving, for instance, (continues}

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HEAD INJURY

(continued)

gunshot wounds to the head, parenchymal damage to the brain is often so extensive that craniotomy is futile (Figure 3). When nonoperative treatment is elected, the goal of management is to maximize cerebral perfusion and oxygen delivery to the brain while preventing or treating complications that may arise. This is accomplished by optimizing the patient's fluid and hemodynamic status, keeping the blood oxygen saturation at almost 100%, and decreasing the intracranial pressure by applying hyperventilation and administering mannitol and/or furosemide. Intracranial pressure measurements are performed in order to maintain pressure as close to normal as possible.

Prognosis Mortality from gunshot head wounds is high. In the largest study of head injuries to date, T. A. Gennarelli and co-authors reported a death rate of 68% for patients With gunshot wounds of the head and 20% for those with stab wounds of the head. The figure for gunshot wounds contrasted markedly with an overall23% mortality for patients with other isolated head injuries. Gunshot wounds of the head represented only 1.6% of trauma center admissions but 10% of deaths. The documented predictors of outcome in cases of head injury are the patient's age, the severity of injury (as measured by the Glasgow coma score), the duration of any post-traumatic amnesia, and the presence or absence of elevated intracranial pressure. Recent studies have suggested correlations between initial CT fmdings (compression (continues}

Figure 3. CT scans of the gunshot patient (Figure 1) demonstrated not only a small entry wound in the right temporal bone (top) but also a large intraparenchymal hematoma, extensive brain edema, and a midline shift to the left (middle). In addition, massive disruption of the skull vertex was visualized at the site of the patient's exit wound (bottom). Hospital Practice September 15. 1992

47

Zanlac • 150 Tablets (ranitldine hydrochloride) Zantac • 300 Tablets (ranitidine hydrochloride) Zantac • Syrup (ranitidlne hydrochloride)

CONDENSED BRIEF SUMMARY

The following is a bnef summary only. Before prescribing, see complete prescribing informatiOn m Zantac" product labeling.

INDICATIONS AND USAGE: Zantac• IS indiCated 10: t. Short-term treatment of active duodenal ulcer. Most patients heal w1th1n 4 weeks. 2. Maintenance therapy for duodenal ulcer patients at reduced dosage after healmg of acute ulcers. 3. The treatment of pathological hypersecretory conditions (e g.. ZoltmgerEilison syndrome and system1c mastocytosis) 4. Short-term treatment of active, benign gastric ulcer. Most patients heal withm 6 weeks and the usefulness of further treatment has not been demon-

strated 5. Treatment of gastroesophageal reflux disease (GERD). Symptomatic relief commonly occurs Within 1 or 2 weeks after starting therapy with Zantac

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150 mg b.1.d. 6. Treatment of endoscopically d1agnosed erosive esophagitis. Healing of endoscopically d1agnosed erosive esophag1t1s occurs at 4 weeks (47%), 8 weeks (71%), and 12 weeks (84%) of therapy w1th Zantac 150 mg q.i.d SymptomatiC relief of heartburn commonly occurs w1thin 24 hours of therapy mittation with Zantac. Concomitant antac1ds should be given as needed for pain relief to pat1ents with act1ve duodenal ulcer: act1ve. bemgn gastric ulcer; hypersecretory states; GERD: and erosive esophagitis. CDNTRAINDICATIONS: Zantac" IS contraindicated for patients known to have hypersensitivity to the drug PRECAUTIONS: General: 1. Symptomatic response to ZantacA therapy does not preclude the presence of gastric malignancy. 2. Smce Zantac is excreted pnmarily by the kidney, dosage should be adjusted in patients with impa1red renal function (see DOSAGE AND ADMINISTRATION). Caution should be observed in patients with hepatic dysfunctmn smce Zantac is metabolized in thehver. laboratory Tests: False-positive tests for urine protein with Multistix• may occur durmg Zantac therapy, and therefore testmg wJth sulfosalicylic ac1d JS recommended Drug Interactions: Although recommended doses of Zantac do not mh1b1t the action of cytochrome P-450 enzymes in the liver, there have been tsolated reports of drug interactiOns that suggest that Zantac may affect the btoava1l· ability of certain drugs by some mechanism as yet unidentified (e.g . a pH· dependent effect on absorption or a change in volume of distribution). Increased or decreased prothrombin t1mes have been reported durmg concurrent use of ranitidine and warfarin. However. m human pharmacokJ· netiC stud1es with dosages of ranitldme up to 400 mg per day. no interactmn occurred: ranil!d1ne had no effect on warfann clearance or prothrombin time. The possibility of an interactmn with warfarin at dosages of ramtidme htgher than 400 mg per day has not been investigated Pregnancy: Teratogenic Effects: Pregnancy Category 8: Reproduction stud· ies have been performed 1n rats and rabbits at doses up to 160 times the human dose and have revealed no ev1dence of impaired fertility or harm to the fetus due to Zantac. There are. however. no adequate and well-controlled studtes m pregnant women. Because animal reproduction stud1es are not always predictive of human response, this drug should be used durmg pregnancy only if clearly needed. Nursing Mothers: Zantac is secreted in human milk. Caution should be exercised when Zantac is admm1stered to a nursing mother. Pediatric Use: Safety and effectiveness in children have not been es· tablished. ADVERSE REACTIONS: Headache, sometimes severe. seems to be related to Zantac• administration. ConstipatiOn. diarrhea. nausea/vomiting, abdominal discomfort/pain, and, rarely, pancreatitis have been reported. There have been rare reports of mala1se. d1uiness. somnolence. insomnia. vertigo. tachycardia, bradycardia, atrioventricular block, premature ventricular beats. and arthralgias. Rare cases of reversible mental confusion, agitation, depression, and hallucinations have been reported, predominantly in severely ill elderly patients. Rare cases of reversible blurred vision suggestive of a change in accommodation have been reported. Rare reports of reversible involuntary motor disturbances have been received. In normal volunteers, SGPT values were increased to at least twice the pretreatment levels in 6 of 12 subjects receiving 100 mg q.i.d. mtravenously for 7 days, and in 4 of 24 subjects receiving 50 mg q.Ld. intravenously for 5 days. There have been occasional reports of hepatJhs, hepatocellular or hepatocanalicular or m1xed. with or without jaund1ce. In such circumstances. ranitidine should be immediately discontinued. These events are usually reversible, but m exceedingly rare circumstances death has occurred Blood count changes (leukopenia, granulocytopema, and thrombocytopenm) have occurred in a few patients. These were usually reversible. Rare cases of agranulocytosis. pancytopema. sometimes w1th marrow hypoplasia,andaplasticanemiaandexceedinglyrarecasesofacquiredJmmune hemolyticanemiahavebeen reported. Although controlled studies have shown no antiandrogemc activity, occasional cases of gynecomastia. impotence. and loss of hb1do have been reported m male patients rece1vmg Zantac, but the incidence did not differ from that in the general populat1on Incidents of rash. mcludmg rare cases suggestive of mild erythema multiforme. and. rarely, alopec1a, have been reported. as well as rare cases of hypersensitivity reactions (e.g., bronchospasm, fever, rash, eosinophilia), anaphylaxis, angioneurotic edema, and small mcreases in serum creatmme. OVERDOSAGE: Information concerning possible overdosage and its treat· ment appears in the full prescnbmg information. DOSAGE AND ADMINISTRATION: (See complete prescnbmg information m Zantac· product labeling.) Dosage Adjustment for Patients With Impaired Renal Function: On the basis of expenence w1th a group of subjects w1th severely impaired renal function treated w1th Zantac. the recommended dosage in patients with a ere· atinine clearan_ce less than 50 ml per m1nute 1s 150 mg or 10 ml (2 tea· spoonfuls eqUivalent to 150 mg of ramlldme) every 24 hours. Should the patient's cond1tion require. the frequency of dosing may be increased to every 12 hours or even further w1th caution Hemodialysis reduces the level of circula_tin_g ranil!dme. Ideally, the do~in~ sche~ule should be ad1us~ed s_o that the llmmg of a scheduled dose comctdes w1th the end of hemod1alys1S. HOW SUPPLIED: Zantac • 150 Tablets (ramM1ne HCI equivalent to 150 mg of ran1tldme) are peach, !Jim-coated, f1ve·s1ded tablets embossed with "ZANTAC 15o·· on one s1de and ··Giaxo" on the other. They are available in bottles of 60 (NDC 0173·0344·42) and 100 (NDC 0173·0344·09) tablets and unit dose packs of 100 (NOC 0173-0344-47) tablets. Zantac • 300 Tablets (ramtldine HCI eqUivalent to 300 mg of ramtldme) are yellow. !Jim-coated, capsule-shaped tablets embossed with "'ZANTAC 3oo·· on one side and "Giaxo" on the other. They are available in bottles of 30 (NDC 0173-0393·40) tablets and unit dose packs of 1DO (NDC 0173·0393·47) tablets Store between 15° and 30°C (59° and 86°F) in a dry place. Protect from light. ReplacecapsecurelyaHereach opening. Zantac• Syrup, a clear. peppermmt-flavored liquid, contams 16.8 mg of ranitJdineHCieQuJvalentto15 mgofranitidineper1 mL1n bottlesof16fluidounces (one pint) (NDC 0173-0383-54) Store between 4c and 25°& (39° and 77°F). Dispense in tight, light-resistant containers as defined in the USP/NF.

HEAD INJURY

or obliteration of either third ventricle or basal cisterns) and low cerebral blood flow soon after injury with poor patient outcome. The harmfulness of physical problems such as posttraumatic seizures is well documented, but post-traumatic psychological disturbances are also now recognized as haVing a profound effect on head-injury surVivors. The behavioral consequences of such disturbances lead to far-reaching familial, societal, and vocational maladjustments. As the understanding of the short- and long-term effects of

head injury has grown, the importance of the first few minutes and hours of management has also been appreciated. Although prevention of these injuries is undoubtedly the best solution, the incidence of penetrating head injury is unlikely to decrease in the foreseeable future. It therefore rests on the primary care provider to become proficient in the principles ofhead-injury management and to assist other professionals in minimizing the disabilities resulting from head injuries. D Dr. Lacqua is a Resident and Dr. Sahdev is Director of Trauma, Department of Surgery, Nassau County Medical Center, East Meadow, N.Y.

Selected Reading Krauss JF et al: The incidence of acute brain injury and serious impairment in a defined population. Am J Epidemiol119: 186, 1984 Gennarelli TA et al: Mortality of patients with head injuries and extracranial injury treated in trauma centers. J Trauma 29: 1193, 1989 American College of Surgeons Committee on Trauma: Advanced Trauma Life Support Course for Physicians. ACS, 1985 Miller MA, Drakontides AB, Leavell LC: The brain and cranial nerves. In Ktmber-Gray-Stackpole's Anatomy and Physiology, 17th ed. Macmillan, New York, 1977, pp 233-252 Gant TD, Epstein LI: Low-velocity gunshot wound to the maxillofacial complex. J Trauma 11: 67 4, 1979 Liekweg WG, Greenfield LJ: Management of penetrating carotid artery injury.AnnSurg 188:587, 1978 Robbs JV, Baker LW. Human RR: Cervico-mediastinal arterial injuries: A surgical challenge. Arch Surg 116: 663, 1981 Mattox KL et al: Prospective MAST study in 911 patients. J Trauma 29:1104, 1989 Ward JD, Becker DP: Head Trauma. In Textbook of Critical Care, Shoemaker WC, Thompson WI, Holbrook PR (Eds). WB Saunders, Philadelphia, 1984, pp926-928 Mendelow AD: The early management of head injury. Curr Opin Neurol Neurosurg4:5, 1991 Barnes MP: Outcome of head injury. Curr Opin Neurol Neurosurg 4:12, 1991

May 1992 2120C

Zantac" 150 Tablets/Zantac" 300 Tablets: G!axo Pharmaceuticals, Research Triangle Park, NC 27709 Zantac~ Syrup: Manufactured for Glaxo Pharmaceuticals, Research Triangle Park, NC 27709 by Roxane Laboratories, Inc., Columbus. OH 43216 .t Copyright 1992, Glaxo Inc. All rights reserved. ZA2493R1 Printed m USA September 1992

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Effective management of penetrating head injury.

Although head injuries are usually easily recognized, other, less obvious lesions should also be promptly investigated. In either case, outcome is oft...
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