LAST MINUTE EMERGENCY MEDICINE - PART 9 docx

CUTANEOUS INJURIES 483 – FIGURE 19-3 — Lund and Browder chart for adults. Moderate burns: (1) partial-thickness burns of 15–25% BSA in low-risk patients, (2) 10–20% BSA in high-risk patients, (3) full-thickness burns of 3–10% BSA; this excludes partial-thickness burns of the hands, face, feet, perineum, or circumferential burns of an extremity. These patients generally require hospitalization Minor burns: (1) partial-thickness burns involving <15% BSA in low-risk patients, (2) 10% in high-risk patients, and (3) full-thickness burns of <2% without other injuries. These patients can be treated as outpatients. Removal of the burning agent and cooling will minimize the burn. However, caution needs to be taken not to cause hypothermia. Airway management can be lifesaving and needs to be performed as early as possible in patients with inhalation injuries or severe extensive burns. All burn patients with exposure to smoke should be placed on 100% humidified oxygen. Fluid resuscitation should be initiated early. Patients with major and moderate burns have extraordinary fluid requirements. There are many methods to estimate the fluid requirements of burn patients. The most commonly used is the Parkland formula (see Table 19-9). The goal of the volume resuscitation should be to maintain a urine output of 0.5–1.0 mL/kg/h. Pain management should be given parentally. Tetanus toxoid should be administered when necessary. Prophylactic antibiotics are not indicated. 484 CHAPTER 19 / TRAUMATIC DISORDERS –FIGURE19-4— Lund and Browder chart: Relative percentage of burns by age. Large wounds should be covered with dry sterile dressings. Small wounds can be covered with saline- soaked dressings to provide cooling and comfort, but caution must be taken to avoid hypothermia. Eventually, small wounds that do not require transfer to a burn center should be dressed with an antibiotic ointment or cream and dry sterile dressings which should be changed twice daily. Blisters should be left intact unless they are large or cross a joint. Devitalized tissue should be debrided to help prevent infection. Circumferential burns of the chest, neck, and extremities may compromise respiration and circulation. Escharotomy may beindicatedto relieve the compromise.If the chest wallis unable to risedue to constriction, incisions are made at the anterior axillary line. Similarly, if extremities have circumferential burns and circulation is compromised, an escharotomy should be performed on the medial and lateral sides. Chemical Burns Definition: Chemical burns are tissue and cellular injury caused by toxins that cause protein denaturation. Etiology: Many different types of chemicals can cause burns. Common agents include lye (drain cleaner), paint removers, disinfectants, bleach, acids, and alkalis. The extent of the injury is determined by (1) con- centration of the agent, (2) manner of contact, (3) quantity of the agent, (4) phase of the agent (i.e., liquid versus solid), (5) duration of exposure, (6) mechanism of action, and (7) extent of skin penetration. The majority of chemical burns are caused by acids or alkalis. CUTANEOUS INJURIES 485 TABLE 19-8 AMERICAN BURN ASSOCIATION BURN UNIT REFERRAL CRITERIA 1. Par tial thickness burns more than 10% total body surface area (TBSA) 2. Burns that involve the face, hands, feet, genitalia, perineum, or major joints 3. Third-deg ree burns in any age group 4. Electrical burns, including lightning injury 5. Chemical burns 6. Inhalation injury 7. Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality 8. Any patients with burns and concomitant trauma (such as fractures) in which the burn injury poses the greatest risk of morbidity or mortality. In such cases, if the trauma poses the greater immediate risk, the patient may be initially stabilized in a trauma center before being transferred to a burn unit. Physician judgment will be necessary in such situations and should be in concert with the regional medical control plan and triage protocols 9. Burned children in hospitals without qualified personnel or equipment for the care of children 10. Burn injury in patients who will require special social, emotional, or long-term rehabilitative intervention Source: American Burn Association, www.ameriburn.org/BurnUnitReferral.pdf. Clinical Presentation: Acids generally cause a coagulation necrosis leading to eschar formation. This eschar prevents deeper skin penetration by the acid. Alkalis, on the other hand, cause a liquefactive necrosis that allows the chemical to penetrate deeper and cause more extensive damage. Extremes of pH cause more damage than more neutral compounds. Diagnosis: Chemical burns may appear deceptively benign. They often appear to have caused minimal damage initially but will get worse over the next 24 hours. Treatment: The goal of treatment is to minimize injury via decontamination and dilution. Some specific agents may require deactivation or neutralization. Dry particulate matter should be brushed away before irrigation is started. Caution should be taken when neutralizing or diluting a chemical, because it may causes an exothermic process that can lead to thermal injury. Sodium metal and related agents should be covered with mineral oil before removal. In general, early irrigation with water improves outcome and minimizes damage. Contaminated clothing should be removed. TABLE 19-9 PARKLAND FORMULA 4mL× wt (kg) × % TBSA of burn = crystalloid fluid in the first 24 h 1 / 2 the volume is given in the first 8 h from the time the burn occurred 486 CHAPTER 19 / TRAUMATIC DISORDERS Most strong acids will produce coagulation necrosis. Acids should be diluted with water; pH paper should be used to monitor the irrigation process. Hydrofluoric (HF) acid produces a unique pattern of injury. It acts like both an acid and alkali. HF penetrates deep into the skin and is extremely painful. Treatment is divided into two phases. Initially, copious irrigation should be instituted. If severe pain persists, then a deeper injury is present. Treatment with calcium gluconate via topical, subcutaneous injection, and IV or intraarterial routes may be required. The elimination of pain can be used to guide therapy and the need for additional treatment. Calcium gluconate 2.5% gel can be applied topically. This gel can be formed by mixing 3.5 g of calcium gluconate powder with 150 mL of water-soluble lubricating jelly. Subcutaneous infiltration is achieved using calcium gluconate 10% at a maximum dose of 0.5 mL/cm 2 of affected skin. Intraarterial injection is achieved by infusing 10 mL of calcium gluconate 10% mixed with 40 mL of D5 W over 4 hours. Initially, alkali burns may appear minor, but since alkalis penetrate much deeper into tissues, the burns may get worse over time and eventually become full thickness. Ingestions of alkalis can be fatal due to early- and late aerodigestive tract injuries. Large amounts of water should be used for dilution because many alkalis (lime) produce exothermic reactions upon dilution. Chemical exposures to the eye are true emergencies and can rapidly lead to loss of vision. Acids cause a cloudy ground glass pupil and tend to be less severe than alkalis. pH paper should be used to determine the acid-base status of the eye. Alkalis cause chemosis, pale conjunctiva, and opacify the pupil. Copious irrigation should be initiated immediately. The pH should be frequently monitored until a pH of 7.4 is achieved. The eye should be irrigated with 1–2 L of normal saline for approximately 30 minutes. Early ophthalmologic consultation is often required. HEAD TRAUMA Closed Head Injury Definition: Primary brain injury refers to the actual traumatic injury or direct blow. Secondary brain injury is the delayed injury that occurs after the initial injury. Etiology: Secondary brain injury results from vascular autoregulatory dysfunction, cerebral edema, and seizures. The most important causes of secondary brain injury that physicians can affect are hypoxia and hypotension. Clinical Presentation: Mild head trauma refers to patients with a Glasgow coma scale (GCS) of 13–15. Moderate head trauma refers to patients with a GCS of 9–12. The Cushing reflex is the clinical syndrome of hypertension, bradycardia, and decreased respiratory effort in patients who are herniating after head trauma. Uncal herniation is the most common herniation syndrome. It is a form of transtentorial herniation and occurs in patients with subdural hematomas (SDHs) or epidural hematomas (EDHs). Compression of the ipsilateral uncus of the temporal lobe on the edge of the tentorium results in compression of the ipsilateral CN III blown pupil and contralateral hemiparesis. In 10–25% of patients, the contralateral pupil is blown. HEAD TRAUMA 487 TABLE 19-10 G LASGOW COMA SC ALE Best motor response Obeys commands 6 Localizes pain 5 Withdraws to painful stimulus 4 Flexion to pain (decorticate posturing) 3 Extension to pain (extensor posturing) 2 No response 1 Best verbal response Oriented and conversant 5 Disoriented 4 Inappropriate words 3 Incomprehensible sounds 2 No response 1 Eyes Opens spontaneously 4 Opens eyes to verbal command 3 Opens eyes to pain 2 No response 1 A concussion is a brief loss of consciousness associated with amnesia, headache, vomiting, but no focal findings. A cerebral contusion is the most common lesion seen on CT in patients with mild head injury. These patients may have mental status changes or coma. The contusion usually involves the frontal and temporal lobes. Patients may have a coup or contrecoup lesion. The treatment is admission for observation. Diagnosis: CT is the diagnostic study of choice for patients with suspected intracranial injury. For patients with minor head injury, CT will be positive in 7–18% of patients; only 1% of patients will have a lesion that requires a neurosurgical procedure. MRI is not sensitive for detecting acute hemorrhage or fractures. It is more sensitive than CT for detecting nonhemorrhagic lesions such as contusions and diffuse axonal injury (DAI) (see Table 19-11). Treatment: The treatment goals for patients with severe head injury (GCS ≤ 8) include early neurosur- gical consultation, airway management, and prevention of secondary brain injury by avoiding hypoxia and hypotension. Other management therapies include hyperventilation, mannitol, and head elevation (once the cervical spine is cleared). The goal of hyperventilation is a PaCO 2 of 30–35 mm Hg. Mannitol is ad- ministered as repeated boluses of 0.25–1 g/kg given over 10–15 minutes. Both of these treatments decrease intracranial pressure (ICP). 488 CHAPTER 19 / TRAUMATIC DISORDERS TAB LE 19 -11 CATEGORIZATIONS FOR I MAG ING IN PATIENTS WITH HEAD TRAUMA Low-risk group (CT not recommended) Asymptomatic Mild headache Dizziness Injury >24 h old Scalp hematoma, abrasion Laceration, contusion Vomiting Moderate-risk group (consider CT) Loss of consciousness (LOC) Amnesia Progressive headache Alcohol or drug intoxication Age <2 yrs and >60 yrs Glasgow corna scale (GCS) <15 High-risk group (CT indicated) Posttraumatic seizure Signs of basilar skull fracture Focal neurologic findings Decreased level of consciousness Coagulopathy Penetrating skull injury Depressed or open skull fracture TABLE 19-12. RAPID SEQUE NCE INTUBATION DR UGS FOR PATIENTS WITH HEAD TRAUMA TABLE 19-13. INDICATIONS FOR SEIZURE PROPHYLAXIS AFTER HEAD TRAUMA TABLE 19-14. INDICATIONS FOR HYPERVENTILATION OF HEAD TRAUMA PATIENTS TABLE 19-15. INDICATIONS FOR MANNITOL ADMINISTRATION FOR HEAD TRAUMA PATIENTS TABLE 19-16. INDICATIONS FOR INTRACRANIAL PRESSURE MONITORING IN HEAD TRAUMA PATIENTS TABLE 19-12 R APID SEQUENCE INTUBATION DRUGS FOR PATIENTS WITH HEAD TRAUMA Pretreatment Vecuronium or pancuronium (0.01 mg/kg) Lidocaine (1.5 mg/kg) Fentanyl (3–5 µg/kg) Paralysis and sedation Etomidate (0.3 mg/kg) Succinylcholine (1.5 mg/kg) Contraindicated Ketamine TABLE 19-13 I NDICATIONS FOR SE IZURE PROPHYLAXIS AFTER HEAD TRAUMA Depressed skull fracture History of seizure after the trauma GCS ≤8 Penetrating injury Subdural, epidural or intracerebral hematoma, subarachnoid hemorrhage TABLE 19-14 I NDICATIONS FOR HYP ERVENTILATION OF HEAD TRAUMA PATIENTS Acute neurologic deterioration Herniation or cerebral edema on CT ICP elevation refractory to other measures (sedation, CSF drainage, osmotic diuresis) TABLE 19-15 I NDICATIONS FOR MAN NITOL ADMINISTRATION FOR HEAD TRAUMA PATIENTS Signs of herniation or increased ICP (on CT or clinical exam) Progressive neurologic deterioration TABLE 19-16 I NDICATIONS FOR I NTRACRANIAL PRESSURE MONITORING IN H EAD TRAUMA PATIENTS GCS ≤8 CT findings of hematoma, contusion, edema, or hydrocephalus 489 490 CHAPTER 19 / TRAUMATIC DISORDERS Subdural Hematoma Definition: Subdural hematomas (SDH) can be acute, subacute, or chronic. Subacute SDHs present after 7 to 25 days postinjury. Chronic SDH refers to one that presents 2 weeks after injury. Etiology: SDHs are due to venous bleeding from disruption of bridging vessels in the subdural space. Patients with brain atrophy are at risk; this includes the elderly and alcoholic patients. SDHs are more common than EDHs. The incidence is 5% of head injury patients and the mortality ranges from 60% to 80%. Clinical Presentation: In the acute setting, patients will have neurologic deficits and headache. Patients with chronic SDH may have few clinical signs or subtle findings such as mental status changes. In the elderly, there may not be a history of trauma. Diagnosis: CT will show the crescent-shaped, hyperdense mass if the SDH is acute. Subacute bleeds appear as isodense masses on CT after 7 to 25 days. In chronic SDH patients, the mass is hypodense (See Figure 19-5). –FIGURE19-5— Subdural Hematoma with midline shift and large scalp hematoma. HEAD TRAUMA 491 Treatment: Neurosurgical consultation should be obtained, and intervention is warranted for patients with neurologic dysfunction. Elderly patients on warfarin require reversal with vitamin K, fresh frozen plasma. Factors VII and IX can be added for faster reversal. Epidural Hematoma Definition: Epidural hematomas (EDH) result from bleeding into the epidural space. Etiology: EDHs result from disruption of the middle meningeal artery from a direct blow to the temporal skull. The incidence is 1–2% of head injuries; mortality rates are 25–50%. Eighty percent are associated with skull fractures. Clinical Presentation: The classic presentation is loss of consciousness followed by a lucid interval, then deterioration. This occurs in less than 30% of patients. Diagnosis: On head CT, an EDH appears as a lenticular, convex mass (see Figure 19-6). Treatment: Immediate neurosurgical consultation and intervention are required. – FIGURE 19-6 — Acute epidural hematoma. Note the lenticular shape and that the bleeding does not cross the suture line. 492 CHAPTER 19 / TRAUMATIC DISORDERS Subarachnoid Hemorrhage Definition: Subarachnoid hemorrhages (SAHs) are the most common types of traumatic intracranial hemorrhages. Etiology: They usually result from a direct blow to the head or as a spontaneous rupture of a congenital intracranial aneurysm. Clinical Presentation: Patients usually have headache and nausea. Diagnosis: CT is the diagnostic modality. Treatment: These injuries do not require surgery, assuming that they are truly traumatic. Use of antiseizure medications is controversial. Many neurosurgeons will favor the use of dilantin to prevent seizures. Diffuse Axonal Injury Definition: Diffuse axonal injury (DAI) results from shearing forces to the brain that cause disruption of axons in the white matter. Etiology: DAI results from rotational trauma to the head. Clinical Presentation: These patients are comatose. The coma usually develops immediately after the trauma. The length of the coma determines the severity of the DAI. Patients with mild DAI are in coma for 6–24 hours. Patients with mild DAI may exhibit posturing on clinical presentation but they usually recover with minimal deficits. Patients with moderate severity DAI have coma for longer than 24 hours and frequently have associated basilar skull fractures. Patients with severe DAI are in coma for longer periods of time and will exhibit posturing as well as autonomic dysfunction. These patients will have elevated intracranial pressure (ICP) due to cerebral edema and may develop herniation. Diagnosis: MRI is required to diagnose DAI. The CT may be normal. Treatment: Neurosurgical consultation iswarranted,butthetreatment is supportive. Patients with evidence of elevated ICP should undergo hyperventilation and osmotic therapy with mannitol. As all of these patients present in coma, airway management is indicated. Skull Fractures Definition: Types of skull fractures include linear, nondisplaced, depressed, open, and basilar skull frac- tures. Clinical Presentation: Patients with basal skull fractures present with hemotympanum, raccoon eyes, rhinorrhea, otorrhea, Battle sign, and cranial nerve deficits Diagnosis: The diagnosis of basal skull fracture is a clinical one. Other types of skull fractures are diagnosed by CT. When a skull fracture is suspected based on scalp wound exploration, CT is indicated to detect potential intracranial hemorrhage. The use of skull films should be reserved for suspected child abuse and asymptomatic infants with scalp hematomas since the majority of intracranial injuries in this age group are associated with skull fractures; skull fractures are associated with scalp hematomas. In addition, in all age groups, skull films may be used in patients with penetrating trauma to locate bullets or other weapons. [...]... spinal cord or nerve roots, or incapacitating deformity or pain TAB LE 1 9- 2 0 TYPES OF CERVICAL SPINE FRACTURES TAB LE 1 9- 2 1 CLINICAL FINDINGS ASSOCIATED WITH SPINAL CORD LEVELS FIGU R E 1 9- 9 CERVICAL SPINE FRACTURES Diagnosis: Nexus low-risk criteria should be used to determine which patients require cervical spine imaging (see Table 1 9- 2 2) The three view plain radiograph is the initial screening test of... the structures at risk are the internal carotid and vertebral arteries – F IGU R E 1 9- 8 — Zones of the neck Reprinted from Baron BJ Penetrating and Blunt Neck Trauma In Tintinalli JE, Kelen GD, Stapczynski JS (eds) Emergency Medicine: A Comprehensive Study Guide 6th ed New York: McGraw-Hill, 2004, p 1 590 , Figure 258–2  499 NECK TRAUMA Diagnosis: For patients with Zone I injuries, diagnostic studies are... require outpatient follow-up with an ENT or plastic surgeon in 3 to 5 days – F IGU R E 1 9- 7 — Le Fort Classification of midface fractures Reprinted with permission from Dingman RO, Natvig P Surgery of Facial Fractures Philadelphia, PA: Saunders, 196 4, p 248 [Pick-up art from Hasan N, Colucciello SA Maxillofacial Trauma In Tintinalli JE, Kelen GD, Stapczynski JS (eds) Emergency Medicine: A Comprehensive... fracture D Odontoid fractures Reprinted from Larson JL Injuries to the Spine In Tintinalli JE, Kelen GD, Stapczynski JS (eds) Emergency Medicine: A Comprehensive Study Guide 6th ed New York: McGraw-Hill, 2004 506 TA B L E 1 9 - 2 2 CHAPTER 19 / TRAUMATIC DISORDERS NEXUS LOW-RISK CRITERIA FOR CERVICAL SPINE IMAGING∗ Patients are at low risk for cervical spine fractures and may be safely spared radiographic... symptomatic patients are listed below When working up the esophagus, due to the high false-negative rate with esophagography, a negative test should be followed up with esophagoscopy Duplex US has a sensitivity as low as 90 % Helical CT angiography has a sensitivity that approaches 100% (see Table 1 9- 1 7) TA B L E 1 9 - 17 DIAGNOSTIC STUDIES FOR PATIENTS WITH PENETRATING NECK TRAUMA Laryngoscopy Bronchoscopy... over 15 minutes then 5.4 mg/kg/h over 23 hours Thoracolumbar Spine Fractures TA B L E 1 9 - 2 3 INDICATIONS FOR THORACOLUMBAR PLAIN RADIOGRAPHS Plain radiographs should be performed for high-energy mechanism patients with the following: Back pain or tenderness Abnormal neurologic examination Other spine fractures GCS . INJURIES 483 – FIGURE 1 9- 3 — Lund and Browder chart for adults. Moderate burns: (1) partial-thickness burns of 15–25% BSA in low-risk patients, (2) 10–20% BSA in high-risk patients, (3) full-thickness burns. open skull fracture TABLE 1 9- 1 2. RAPID SEQUE NCE INTUBATION DR UGS FOR PATIENTS WITH HEAD TRAUMA TABLE 1 9- 1 3. INDICATIONS FOR SEIZURE PROPHYLAXIS AFTER HEAD TRAUMA TABLE 1 9- 1 4. INDICATIONS FOR HYPERVENTILATION. PATIENTS TABLE 1 9- 1 5. INDICATIONS FOR MANNITOL ADMINISTRATION FOR HEAD TRAUMA PATIENTS TABLE 1 9- 1 6. INDICATIONS FOR INTRACRANIAL PRESSURE MONITORING IN HEAD TRAUMA PATIENTS TABLE 1 9- 1 2 R APID SEQUENCE