Trauma in Pregnancy 499 regulation described above. Unfortunately, reperfusion of the injured area may occur in the presence of absent or diminished autoregulation. Injury is either mechanically (through edema) or metabolically (through inappropriate substrate production) pro- duced through reperfusion [117] . In order to avoid or limit permanent cerebral injury, specifi c cerebral resuscitation must be carried out in the head trauma victim. The sooner resuscitation is begun, the greater the chance injured, but living, neuronal tissue will survive [117 – 119] . Brain i njury m echanism in t rauma Penetrating head injuries produce injury by obvious mechanisms. With blunt head trauma, especially in deceleration events, move- ment of the brain occurs fi rst in one direction with a secondary rebound movement in the opposite direction producing a coup – countercoup effect. Closed head injuries can occur without signifi - cant injury of the cutaneous tissues and calvarium through bruising or contusion of the brain at coup or countercoup sites. Intracerebral hemorrhage from traumatic brain injury often results from severe contusion. Subdural or epidural hematomas are produced by direct laceration or tearing of subdural or epidural vessels, respectively [6,116] . Primary m anagement of t raumatic b rain i njury Initial management of suspected brain injury starts with the basic “ ABCs ” discussed previously. Profound hypotension, defi ned as systolic blood pressure less than 60 mmHg in non - pregnant indi- viduals, may cause or contribute to altered consciousness. Correction of hypotension is important. While possible, hypo- tension as a result of the neurologic insult is uncommon. Until proven otherwise, hypotension in the presence of head injury is usually from other causes. Severe hypertension in the comatose trauma victim may be centrally mediated. This “ Cushing response ” is also characterized by bradycardia and a diminished respiratory rate [113] . Altered levels of consciousness may also be produced by alcohol or drug ingestion. Toxicological assessment is recommended in most trauma patients with altered levels of consciousness. Conversely, an altered level of consciousness should never be totally attributed to alcohol or other drug inges- tion alone unless completely proven otherwise. Finally, other medical conditions such as hypoglycemia may occasionally be seen coincidental with trauma. A baseline and ongoing mental assessment is necessary as a frame of reference in all trauma patients. The “ A - V - P - U ” mini exam (Figure 37.1 ) is a brief primary survey tool. In the secondary survey, more extensive evaluation, such as by the Glasgow Coma scale (GCS) is recommended (Table 37.2 ) [15,16] . A score of 8 or less is indicative of the diagnosis of coma and is classifi ed as severe head injury [6,114,118] . If the GCS is from 9 to 12, the injury is classifi ed as moderate. GCS scores greater than 12 are classifi ed as minor head injuries [108,116] . Once again, the GCS and other neurologic examinations need to be performed fre- quently so trends in neurologic response can be identifi ed. A decrease in the GCS score of 2 or more points is indicative of Head t rauma Approximately 50% of all trauma deaths are associated with head injury. Over 60% of motor vehicle - associated trauma deaths occur as a result of head trauma [6] . In a recent review of preg- nant trauma deaths in Cook County (Illinois), approximately 10% of maternal trauma deaths were directly due to head injury [112] . Several aspects of cranial and cerebral physiology and patho- physiology are very important in head trauma victims. The brain is one of the most carefully protected organs of the body; the calvarium and cerebrospinal fl uid cushion the brain from minor trauma. However, in severe trauma, these two otherwise protec- tive features may contribute to or precipitate brain injury. The brain has poor tolerance of diminished perfusion with little or no metabolic reserve in brain tissues. Global cerebral oxygen con- sumption of at least 1.5 mL/100 g/min must be maintained to prevent injury. Oxygen delivery to the brain is determined by blood pressure, blood oxygen content, blood fl ow distribution, and relative perfusion pressure. Because the closed space of the calvarium is occupied by blood, cerebrospinal fl uid, and brain volume, intracranial pressure is a function of all three compo- nents, referred to as the Monro – Kellie doctrine. Cerebral edema results in increased brain volume, thereby producing elevated intracranial pressure. Traumatic collections of blood in the cranial vault will similarly increase intracranial pressure. Often, both of these mechanisms are present in the head trauma victim [113,114] . Cerebral a utoregulation in t raumatic i njury Cerebral autoregulation is normally maintained over a wide range of blood pressures. Extremes of blood pressure, such as hypotension found in the multiple trauma victim, taxes the brain ’ s ability to autoregulate. When coupled with cerebral edema and/or intracranial bleeding, hypotension further aggra- vates the inability of the brain to autoregulate. When the injured brain loses its ability to autoregulate, self - perpetuation of the brain injury occurs. Finally, because the cranium is a closed system, propagation of elevated extravascular cerebral pressure transmurally causes the driving pressure in the cerebral circula- tion to be signifi cantly decreased. In that fl ow is directly deter- mined by a change in pressure, diminished cerebral perfusion pressure (mean arterial blood pressure – intracranial pressure) causes decreased effective cerebral blood fl ow. Cerebral mass lesions will therefore diminish cerebral perfusion pressure in pro- portion to their size even in the face of normal blood pressure. It should thus be obvious that acute brain injury is often self - perpetuating and when in evolution and is poorly tolerated by the fastidious neuronal cells. Cell death and permanent injury may result. The therapeutic goal of acute cerebral resuscitation is to limit cell death by regulated reperfusion to non - functioning, but still viable brain tissue ( ischemic penumbra ). The clinician ’ s ability to accomplish this goal is often limited [115,116] . Another feature of brain injury is the concept of secondary, or reperfusion, injury. An initial insult produces the loss of auto- Chapter 37 500 at least 24 hours [120] . Other criteria that differentiate mild con- cussion (less likelihood of sequelae) from the more severe classic concussion include the presence or absence of loss of conscious- ness itself, the duration of amnesia, and the presence of persistent memory defi cit. Diffuse axonal injury (DAI), more commonly known as “ closed head injury ” , is produced by widespread global brain injury or the cerebral edema resulting from diffuse brain injury [118] . Prolonged coma is the hallmark of DAI. CT imaging will show cerebral edema without focal lesions. Nearly 50% of coma - producing brain injuries are caused by DAI. DAI is classi- fi ed clinically into mild, moderate, and severe categories [121] . Severe DAI carries a 50% mortality. Long - term supportive care and control of intracranial hypertension are the only treatment for the condition. Partial or complete recovery is possible, but permanent coma ( “ chronic vegetative state ” ) is often an inexo- rable consequence of severe DAI. Focal b rain i njury Focal brain injuries are those in which damage occurs in a rela- tively local area. Types of focal brain injury include contusions, hemorrhages, and hematomas. Because focal injuries may produce a mass effect and damage underlying normal brain tissue, rapid diagnosis and treatment of focal brain injuries may improve outcome and recovery. Contusions are usually caused by deceleration coup – counter- coup trauma as previously described. Although contusions can occur anywhere, they are most commonly found in the tips of the frontal and temporal lobes. In addition to producing defi cits from focal injury, delayed bleeding and edema can produce injury from mass effects [116] . Prolonged observation is recommended. If neurologic deterioration is detected and is thought to be from a mass effect, surgery may be indicated. Hemorrhages and hematomas can be functionally classifi ed into those occurring in the meningeal or parenchymal regions of the brain. Parenchymal hemorrhage includes intracerebral hema- tomas, impalement injuries and missile (bullet) wounds. Meningeal hemorrhage is further classifi ed as acute epidural hemorrhage, acute subdural hematoma, or subarachnoid hemorrhage. Acute epidural hemorrhage (AEH) usually occurs from tears in the middle meningeal artery. Although found in 1% or less of coma - producing acute brain injuries, AEH can be rapidly pro- gressive and fatal. Figure 37.3 describes the usual sequence of events associated with AEH. It is important to note that the patient with AEH may display an intervening period of lucidity prior to a rapid deterioration from massive rebleeding of the lesion [143] . If surgically treated early, the prognosis is good (91% survival) [118] . If not evacuated until hemiparesis and pupil fi xation, the prognosis is poor. AEH is, in effect, “ the vasa previa ” of acute brain injury. Rapid recognition and treatment yields markedly improved results. Subarachnoid hemorrhage (SAH) produces bleeding in the subarachnoid space. Meningeal irritation occurs with the result- ing symptoms of headache and/or photophobia. Because the sub- deterioration [108] . Irrespective of the GCS score, unequal pupils, unequal motor fi ndings, open head injury with leaking cerebro- spinal fl uid or exposed brain tissue, and/or the presence of a depressed skull fracture also indicate severe head injury. Finally, if headache severity dramatically increases, pupillary size increases unilaterally, or lateralizing weakness is noted to develop, particu- lar concern is warranted. Appropriate immediate investigations of the head trauma victim may include roentgenograms (X - ray), CT radiography, and neurologic or neurosurgical consultation. Sedation and/or paralysis is delayed until the consultant examines the patient, if possible. Generally, all patients with moderate or severe head injury should be radiographically evaluated for cervical spine fracture. Conversely, skull roentgenograms are often not helpful [108] as physical examination or CT imaging provide more reli- able information and higher - quality data. CT imaging is a vital tool in the evaluation of head injuries and except for women with minor injuries, all head - injured patients require CT imaging. Severe injury dictates imaging as soon as possible. However, it is important to adequately monitor the victim while she undergoes imaging. Once C - spine fractures are ruled out, the 20+ week gestation pregnant patient is placed in left lateral tilt during the scanning [9] . Head injuries can be simply classifi ed into the cat- egories of diffuse brain injury, focal brain injury, and skull frac- tures (Table 37.4 ) [6,8,116] . Diffuse b rain i njury Diffuse brain injury can be classifi ed as a concussion or diffuse axonal injury. Concussion is produced from widespread brief interruption of global brain function. Although confusion, head- ache, dizziness, etc., are often present in the recovering concus- sion victim, any persistent neurologic abnormalities in the patient with a presumed concussion must be investigated for other eti- ologies. Many authors feel that the patient with 5 minutes or more of lost consciousness should be observed in the hospital for Table 37.4 Classifi cation of acute head trauma. Diffuse brain injury A. Concussion B. Diffuse axonal injury Focal brain injury A. Contusion B. Hemorrhage/hematoma 1. Parenchymal hemorrhage 2. Meningeal hemorrhage/hematoma a. Acute epidural hemorrhage/hematoma b. Subarachnoid hemorrhage/hematoma Skull fractures A. Simple fracture B. Basilar skull fracture C. Depressed skull fracture Trauma in Pregnancy 501 Basilar skull fractures may not immediately be apparent clinically. Anterior basilar skull fractures may predispose to inadvertent placement of a nasogastric tube into the intracranial space [116] . Skull fractures typical require cranial CT scanning and physical exam. Skull X - rays are usually not helpful for the initial evalua- tion of head injury. Attempt at precise delineation of skull frac- tures should not delay recognition and treatment of other head injuries. Head t rauma: g eneral p rinciples Mainstays in the treatment of head trauma include maintenance of brain perfusion, reduction of cerebral edema, elimination or reduction of hemorrhage, and prevention of infection. Patients with evolving symptomatology or unremitting coma need to be evaluated immediately for potential neurosurgical intervention. Maintenance of normal arterial blood pressure will aid the often impaired cerebral autoregulation seen with head trauma. Normalization of blood glucose will help supply cerebral meta- bolic needs. Hyperglycemia is to be avoided, as it is as undesirable as hypoglycemia [114,120] . Figure 37.5 outlines a general scheme for severe head injury triage and features of high - , moderate - , and low - risk lesions. It should be noted that a lateralizing defect and GCS ≤ 8 requires immediate evaluation for surgical treatment. Intracranial pres- sure (ICP) monitoring has been long advocated as a measure to improve outcome in traumatic brain injury. There is clearly a split of opinion with regard to the indications and effectiveness of ICP monitoring. The current consensus recommendations propose ICP monitoring be used in comatose patients with GCS scores of 8 or less after resuscitation who also demonstrate patho- logic CT radiographic abnormalities. In those patients with a GCS of 8 or less without CT abnormalities, ICP monitoring is indi- cated if two or more of the following are present: age > 40 years, unilateral or bilateral posturing, and systolic blood pressure less than 90 mmHg at any time since injury [117,126,127] . Abnormal intracranial pressure (ICP) is medically treated with controlled hyperventilation, mannitol administration, barbiturate coma, loop diuretics, volume restriction, and head - up positioning [117] . When ICP monitoring is employed, measurements above 20 – 25 mmHg generally necessitate treatment strategies to lower ICP. Hyperventilation works to transiently decrease ICP by reduc- ing cerebral blood fl ow. If used, hyperventilation should be undertaken to a P a CO 2 endpoint of 26 – 28 mmHg [128] , although the appropriate level for pregnancy is not established. Hyperventilation is not effective in “ prophylaxis ” against elevated ICP [6,112,129] . If hyperventilation is abruptly discontinued, ICP may rise rapidly. Current data refute the long - held clinical practice of using aggressive hyperventilation for the treatment or prevention of intracranial hypertension. In non - pregnant patients, sustained hyperventilation is associated with the least favorable outcome. Hyperventilation ’ s impact is probably medi- ated through reduction in cerebral blood fl ow in normal brain parenchyma surrounding damaged neural tissue. Hyperventilation arachnoid space is much larger than the epidural space, bleeding does not usually rapidly progress to death. Although bloody spinal fl uid is a hallmark of SAH, CT scanning has basically replaced lumbar puncture in the diagnosis of SAH. Evacuation is sometimes not required. If evacuation is not performed, treat- ment is supportive. Meningeal irritation can produce unwanted cerebral artery vasospasm. Cerebral artery vasospasm may be diagnosed by clinical ascertainment of neurological defi cit, with either empiric treatment and/or confi rmation via transcranial Doppler velocitometry and/or cerebral arteriography. Treatment of cerebral artery vasospasm involves volume loading, vasopres- sor - induced hypertension and calcium channel blocker therapy with nimodipine. Refractory treatment of vasospasm has been advocated by the use of angiographically instilled papaverine and/ or calcium channel blocking agents or direct balloon angioplasty [114,119,122] . Clear - cut consensus on optimal treatment is still pending [123] . Acute subdural hematoma (SDH) is one of the more common causes of serious brain hemorrhage. SDHs commonly occur from rupture of bridging veins between the cerebral cortex and dura; but, may also occur from direct laceration of the brain or cortical arteries. The clinical presentation of SDH often depends upon the rapidity of expansion of the hematoma. Rapidly expanding hematomas carry a poorer prognosis than do stable, chronic SDHs. Early evacuation of rapidly growing SDHs may favorably impact the 60% mortality that SDH carries [20,118,120] . Others advocate early (within 4 hours of injury) evacuation of subdural hematomas greater than 1 cm in diameter that are associated with a shift in midline brain structures. Patients with subdural hema- tomas of less than 5 mm with only mild or absent neurologic symptoms may be candidates for expectant management. Intracerebral hematomas can occur anywhere in the brain. Symptoms and outcome depend upon the size and location. Intraventricular and intracerebellar hemorrhages portend poor outcome. With impalement injuries the missile or projectile should be left in place until neurosurgical evaluation is obtained. Bullet wounds should be mapped as to entrance and potential exit. CT radiography may help the localization process of any remaining missile fragments. Non - penetrating bullet wounds may result in signifi cant blunt trauma [118,125] . Skull fractures are relatively common and may or may not be associated with severe brain injury. Because skull fractures may be an indicator that signifi cant energy dispersal occurred on the cranial vault, most patients with seemingly uncomplicated skull fractures should still be observed in the hospital with serial neu- rosurgical evaluations. Skull f ractures Different types of skull fractures have different clinical consider- ations. Linear non - depressed skull fractures that traverse suture lines or vascular arterial grooves may be associated with epidural hemorrhage, whereas depressed skull fractures may require oper- ative elevation of the bony fragment. On the other hand, open skull fractures nearly always require early operative intervention. Chapter 37 502 mannitol is used in severe head trauma, the benefi ts of its admin- istration far outweigh these risks [9,116] . Diuresis with furose- mide or other loop diuretics may also be used. Overhydration, especially with hypotonic solutions, should be avoided. Head - up positioning at 20 ° may marginally reduce hydrostatic pressure. Barbiturate coma has been utilized as a treatment of refractory intracranial hypertension. The technique probably works by reducing cerebral oxygen consumption [118,119] . Corticosteroids are not indicated for therapy of cerebral edema from trauma [120,131] . Other less successful treatments of refractory intracra- nial hypertension include hypothermia, decompressive craniot- omy, hypertonic saline, and a variety of investigational neuroprotective agents. Research is ongoing in this area of neurotrauma. Delivery c onsiderations in b rain t rauma The best route of delivery in the patient with acute brain injury is unknown [132] . The original large series addressing the issue in patients with non - traumatic brain injury was in 1974 by Hunt et al. [132] . Regardless, limited data are available as to the recom- is no longer recommended and should be avoided, if possible, within the fi rst 24 hours following acute brain injury. If used at all, the technique is reserved for temporary treatment of severe intractable intracranial hypertension. The effects of normal preg- nancy (compensated respiratory alkalosis) on CO 2 - mediated regulation of cerebral blood fl ow are not known. Mannitol functions as a hyperosmotic diuretic. Doses of 0.5 – 1 g/kg body weight are typically used as primary treatment of intracranial hypertension [130] . Frequent monitoring of serum osmolality is needed, and mannitol should be withheld if osmo- lality is greater than 315 – 320 mOsm/L. Treatment may be directed at maintaining ICP at less than 20 – 25 mmHg. Alternatively, cere- bral perfusion pressure - directed treatment (CPP = mean arterial pressure – ICP) may be instituted using mannitol and peripheral vasoconstrictors to increase mean peripheral arterial pressure. At present, there is no standard recommendation for CPP nor is there a recommendation as to the most effective way for achiev- ing a particular CPP treatment endpoint. Mannitol can theoreti- cally affect uteroplacental perfusion and/or fetal volume homeostasis. However, given the grave circumstances for which Survey for other injuries General resuscitation Cranial computed radiography (CCR)* Glascow coma scale (GCS) scoring GCS ≥9 GCS ≤8 Intracranial pressure monitoring may not be indicated unless specifically warranted Intracranial pressure monitoring** CCR with defect 2 or more not present: • >40 years of age • Posturing • Systolic BP <90 mmHg 2 or more present: • >40 years of age • Posturing • Systolic BP <90 mmHg CCR without defect Figure 37.5 Initial evaluation of the comatose trauma victim. * Neurosurgical consultation liberally indicated during the evaluation of the comatose trauma victim. * * A lateralizing defect with GCS < 8 may necessitate expedited surgical exploration (sources as referenced in text). Trauma in Pregnancy 503 fracture should be accomplished relatively early. The underlying rationale is that outcome is improved in the stable head injury patient when the femur fracture is addressed within 3 – 5 days after the injury [136] . Placement of pins to stabilize fractures does not appear to increase the incidence of acute respiratory distress syn- drome (previously held opinion was that embolic marrow show- ering occurred as a consequence of bone manipulation from hardware placement ). One serious manifestation of severe injury of extremities is acute, compartment syndrome (ACS) . ACS is causes by tissue edema and/or bleeding increasing the intramural pressure within a fascial compartment. ACS is not an infrequent complication of traumatic skeletal injury. Up to 17% of patients with a tibial fracture secondary to a motor vehicle accident may develop ACS [137] . Clinical features of the diagnosis include severe pain, ten- derness, and swelling of the involved extremity. Loss of distal pulses is a late fi nding. Tonometry of an affected fascial compart- ment may be used to supplant clinical diagnosis. Treatment is by fasciotomy, and, outcome is improved if the diagnosis is made early [138] . As stated previously, published experience with the specifi c management of traumatic orthopedic injury in pregnancy is lacking. However, the general principles discussed in this section may serve to provide a basis of management during pregnancy. Multidisciplinary care is helpful in the management of complex cases. Spinal t rauma in p regnancy Spinal cord injury has both immediate and long - term implica- tions for trauma victim. As related earlier in this chapter, neck and back stabilization is paramount during the extraction, trans- port, and initial resuscitative phases of any patient with suspected neck or back injury. Use of back boards and neck stabilization during intubation are crucial to the preservation of whatever potential function remains and for the prevention of further spinal cord trauma. As with other traumatic injury, avoidance of systemic hypotension is associated with better neurological outcome after traumatic spinal injury. Suspected neck or back traumatic injury necessitates both cer- vical spine radiography and careful evaluation of the spine via CT radiography. When specifi c radiographic screening techniques are utilized, the combination of three - view cervical spine X - ray and CT radiography have an over 99% negative predictive value in ruling out signifi cant spinal injury [139,140] . Identifi ed inju- ries need to be stabilized under the care of a skilled neurosurgeon. Surgical strategy in these cases is beyond the scope of this text. Opinion is divided regarding early (postresuscitation and imme- diate treatment of acutely life - threatening injuries) surgical repair of spinal cord injury patients. Another unanswered question is that concerning the use of corticosteroids. Several randomized and non - randomized trials have been conducted in order to answer the question as to whether systemic corticosteroid admin- istration results in improved neurological outcome in traumatic spinal injury. Opinion is divided over corticosteroid use in blunt mended route of delivery in patients with traumatic or atraumatic brain injury. Individualized therapy and consultation with a neu- rologist and/or a neurosurgeon are recommended. Rapid diagnosis, early neurosurgical intervention and meticu- lous attention to support measures offer the best hope for a favorable outcome in patients with severe brain injuries. Comanagement with consultants, appropriate and timely use of cranial CT scans, and serial neurologic examination may reduce mortality and morbidity in brain trauma. Improvement in mater- nal outcome offers the best hope for improved fetal outcome. Traumatic o rthopedic i njury Very limited information has been published specifi cally on frac- ture management complicating pregnant traumatic injury. Just as the care of a complicated pregnancy requires the expertise of a qualifi ed obstetrician and gynecologist or maternal - fetal medi- cine subspecialist, specifi c management of skeletal fractures is beyond the scope of this text and warrants specifi c management by the appropriately trained and credentialed orthopedic special- ist. However, several important points and issues may help the obstetric provider care for the pregnant trauma patient with mul- tiple fractures. In the initial assessment of the victim with orthopedic injury, only acute extremity injury and unstable pelvic fracture with fracture - related hemorrhage are typically immediate life - threat- ening injuries which would require emergency department or immediate operating room treatment [133] . Acute extremity hemorrhage is managed according to the site of hemorrhage and degree of bleeding and the injury itself. An unstable pelvic frac- ture or dislocation may result in marked pelvic hemorrhage. If faced with a patient with an unstable bleeding pelvic fracture, most orthopedic specialists recommend placement of an external pelvic fi xator to reduce pelvic volume and to stabilize the pelvic ring. Hemorrhage is generally controlled so as to allow successful resuscitation and focus on other injuries [134] . Other chapters of this book outline the importance of deep venous thrombosis (DVT) prophylaxis: DVT prophylaxis is very important in the patient with orthopedic injury. Orthopedic urgencies (after and/or not at the exclusion of primary resuscitation and life - saving measures) generally include management of amputation or devascularization, and debride- ment of open fractures. Necessity for amputation of the severely mangled extremity is directly related to the age of the victim, the degree of skeletal or soft tissue injury, the degree of systemic hypotension/shock, and the degree of and duration of limb isch- emia. Re - attachment of a severed limb is possible and should be considered as appropriate after primary stabilization has occurred [135] . Open fracture debridement and fi xation will help relieve pain and may improve long - term outcome. Early, but non - immediate fracture fi xation allows earlier mobilization. Fixation and repair of a femur fracture is usually not an immediate concern during resuscitation of the trauma victim with a concomitant head injury. However, it is recommended that repair of the femur Chapter 37 504 3 Fildes J , Reed L , Jones N , Martin M , Barrett J . Trauma: the leading cause of maternal death . J Trauma 1992 ; 32 : 643 . 4 Sachs BP , Brown DAT , Driscoll SG , et al. Maternal mortality Massachusetts: trends and prevention . N Engl J Med 1987 ; 316 : 667 . 5 Satin A , Hemsell DL , Stone IC , et al. Sexual assault in pregnancy . Obstet Gynecol 1991 ; 77 : 710 . 6 American College of Surgeons, Committee on Trauma . Advanced Trauma Life Support , 7th edn. Chicago : First Impressions , 2004 . 7 Vaizey CJ , Jacobson MJ , Cross FW . Trauma in pregnancy . Br J Surg 1994 ; 81 : 1406 . 8 American College of Surgeons . Advanced Trauma Life Support for Doctors – Faculty Manual , 7th edn. Chicago : First Impressions , 2004 . 9 Kuhlman RS , Cruikshank DP . Maternal trauma during pregnancy . Clin Obstet Gynecol 1994 ; 37 : 274 . 10 Scorpio RJ , Esposito TJ , Smith LG , Gens DR . Blunt trauma during pregnancy: factors affecting fetal outcome . J Trauma 1992 ; 32 : 213 . 11 Hoff WS , d ’ Amelio LF , Tinkhoff GH , et al. Maternal predictors of fetal demise during pregnancy . Surg Gynecol Obstet 1991 ; 172 : 175 . 12 Dilts PV , Brintzman CR , Kirschbaum TH , et al. Uterine and sys- temic hemodynamic inter - relationships and their response to hypoxia . Am J Obstet Gynecol 1967 ; 103 : 38 . 13 Greiss F . Uterine vascular response to hemorrhage during preg- nancy . Obstet Gynecol 1966 ; 27 : 408 . 14 Hankins GDV , Barth WH , Satin AJ . Critical care medicine and the obstetric patient . In: Ayres SM , Grenuik A , Holbrook PR , Shoemaker WC , eds. Textbook of Critical Care , 3rd edn. Philadelphia : WB Saunders , 1995 : 50 – 64 . 15 Jennett B , Teasdale G , Braakman R , et al. Prognosis of patients with severe head injury . Neurosurgery 1979 ; 4 : 283 . 16 Teasdale G , Jennett B . Assessment of coma and impaired conscious- ness: a practical scale . Lancet 1974 ; 1 : 81 . 17 Baxt WG , Moody P . The differential survival of trauma patients . J Trauma 1987 ; 27 : 602 . 18 Rutherford EJ , Nelson LD . Initial assessment of the multiple trauma patient . In: Ayres SM , Grenuik A , Holbrook PR , Shoemaker WC , eds. Textbook of Critical Care , 3rd edn. Philadelphia : WB Saunders , 1995 : 1382 – 1389 . 19 Winchell RJ , Hoyt DB , Simons RK . Use of computed tomography of the head in the hypotensive blunt - trauma patient . Ann Emerg Med 1995 ; 25 : 737 . 20 National Blood Transfusion Service Immunoglobulin Working Party . Recommendations for the use of anti - D immunoglobulin . 1991 : 137 – 145 . 21 Pearlman MD , Tintinalli JE , Lorenz RP . Blunt trauma during preg- nancy . N Engl J Med 1990 ; 323 : 1609 . 22 Goodwin TM , Breen MT . Pregnancy and fetomaternal hemorrhage after noncatastrophic trauma . Am J Obstet Gynecol 1990 ; 162 : 665 . 23 Rose PG , Strohm PL , Zuspan FP . Fetomaternal hemorrhage follow- ing trauma . Am J Obstet Gynecol 1985 ; 153 : 844 . 24 Bowman JM . Management of Rh - isoimmunization . Obstet Gynecol 1978 ; 52 : 1 . 25 Laml T , Egermann R , Lapin A , Zekert M , Wagenbichler P . Feto - maternal hemorrhage after a car accident: a case report . Acta Obstet Gynecol Scand 2001 ; 80 : 480 . 26 American College of Obstetricians and Gynecologists . Practice Bulletin No. 282. Prevention of RhD Alloimmunization . Washington, DC : American College of Obstetricians and Gynecologists , 1999 . spinal injury [140,141] . It does appear that corticosteroids are not benefi cial in penetrating spinal injury (such as gunshot wounds) [142] . If used at all, therapy should be begun within 8 hours fol- lowing injury. Several manifestations of autonomic instability may be seen in the spinal injury victim. The patient with recent cervical or tho- racic spinal cord complete transection has a loss of sympathetic outfl ow. Vagal afferent and efferent innervation is preserved through the intact vagus nerve, with the result being systemic hypotension and bradycardia from unbalanced parasympathetic stimulation. Heat dissipation increases and oliguria may result. Initial treatment with isotonic fl uid resuscitation may not be totally effective. Vasopressors and/or pressor inotropes (dopa- mine) may be required. In the non - pregnant patient, a target mean arterial blood pressure (MAP) of at least 85 – 90 mmHg is optimal for best neurologic outcome [140,143] . Since published data are limited in pregnant populations, individualized guidance using fetal heart rate monitoring in the potentially viable fetus may be required. In the non - acute setting, incomplete transections above T5 through T6 may place the patient at risk from autonomic dysre- fl exia. Afferent stimulation from a hollow viscus often produces marked catecholamine release with marked hypertension and other sympathetic sequelae. Uterine stimulation from labor, bladder distention, constipation, or superfi cial stimulation of the skin below the level of the lesion may produce this condition [144,145] . For the laboring patient, epidural or spinal anesthesia may ameliorate the unopposed afferent stimulation. Treatment of hypertension via direct - acting agents or ganglionic blockade may be necessary in patients who do not have epidural or spinal anesthesia [140] . Long - term care of the patient with a catastrophic spinal injury is beyond the aim of this chapter. Severe impairment may result in lifelong challenges for the spinal injury victim. Conclusion Trauma during pregnancy poses a special and immediate chal- lenge to the obstetrician and to the emergency room provider. Generally speaking, most diagnostic and therapeutic modalities relating to trauma care should not be avoided or modifi ed during pregnancy. Co - management, with input from obstetric and non - obstetric services, functions to insure appropriate care of the pregnant trauma victim and her fetus. References 1 Laverly JP , Staten - McCormick M . Management of moderate to severe trauma in pregnancy . Obstet Gynecol Clin North Am 1995 ; 22 : 69 . 2 Vainer MW . Maternal mortality in Iowa from 1952 to 1986 . 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J Neurosurg 1978 ; 48 : 689 . 508 Critical Care Obstetrics, 5th edition. Edited by M. Belfort, G. Saade, M. Foley, J. Phelan and G. Dildy. © 2010 Blackwell Publishing Ltd. 38 Thermal and Electrical Injury Cornelia R. Graves Tennessee Maternal - Fetal Medicine PLC, Nashville, and Vanderbilt University, Nashville, TN, USA Introduction Most burns are caused by exposure to a thermal, chemical, or electrical source. Recent studies have estimated that approxi- mately 7% of women of reproductive age are seen for treatment of major burns. In the United States, most burns during preg- nancy are due to industrial accidents [1] . Unfortunately, a recent proliferation of clandestine methamphetamine labs, especially in rural areas, has emerged as a new cause of burns in this age group [2] . Maternal and perinatal morbidity and mortality increase as the total body surface area burned increases [3 – 5] (Figure 38.1 ). In the non - pregnant population, recent advances in treatment have reduced mortality rates and improved the quality of life in burn survivors. This has been translated into improved survival for both mother and fetus. Due to the complicated clinical nature of the process, a multidisciplinary approach is required to achieve the best results. Classifi cation Burns are classifi ed by degree based on the depth of the burn into the skin and also by the amount of surface area involved. Partial - thickness injury includes fi rst - and second - degree burns; third - degree burns are full thickness. First - degree or superfi cial burns involve the epidermis only. The skin is erythematous and painful to touch. The best example of this type of burn is a sunburn. These types of burns require topical treatment only. Second - degree burns involve death and destruction of portions of the epidermis and part of the corium or dermis. A superfi cial burn is typically characterized by fl uid - fi lled blisters. A deep partial - thickness burn may form eschar. On initial evaluation, it may be diffi cult to assess the depth of the injury. These burns are painful, but enough viable tissue is left for healing to take place without grafting. Third - degree or full - thickness burns involve the dermis and the corium (dermis) and extend into the fat layer or further. The skin has a thick layer of eschar and may or may not be painful depending on the amount of damage done to the surrounding nerves [3] . In addition to the thickness of the burn, the part of the body burned, concurrent injuries, and past medical history may also affect outcome. Estimation of total body surface area (TBSA) involved in a burn may be determined in two ways: “ the rule of nines ” or the Lund – Browder chart [6] . The rule of nines divides the body into sections that allows for quick estimation of the burn area and is especially useful in emergency situations (Table 38.1 ). The Lund – Browder chart also divides the body into sections but is more accurate as it takes into account changes in body surface area related to patient age. In both methods only second - and third - degree burns are estimated. A chart specifi c to pregnancy has not been developed [6] . Minor burns involve less than 10% of TBSA, are no more than partial thickness in depth, and are otherwise uncomplicated. Burns are considered major if the patient has a history of chronic illness, if the burn involves the face, hands, or perineum, if there is concurrent injury, or if the burn is caused by electrical injury [7] . Critical burns encompass greater than 40% of TBSA and are associated with major morbidity and mortality. Severe burns involve 20 – 39% of TBSA; moderate burns involve 10 – 19% of TBSA [8] . Thermal b urns Thermal injuries during pregnancy usually occur at home and are most often caused by fl ame burns or hot scalding liquids. This type of burn commonly involves smoke inhalation injury. The burn only involves the area of the body that was in direct contact with the cause of the injury. Thermal burns are classifi ed based on the degree of injury as described above [3,9] . . GDV , Barth WH , Satin AJ . Critical care medicine and the obstetric patient . In: Ayres SM , Grenuik A , Holbrook PR , Shoemaker WC , eds. Textbook of Critical Care , 3rd edn. Philadelphia. of Critical Care . Philadelphia : WB Saunders , 1995 : 1449 – 1457 . 119 Brain Trauma Foundation, American Association of Neurological Surgeons , Joint Section on Neurotrauma and Critical Care. . sympathomimetic tocolytic agents . In: Clark SL , Cotton DB , Hankins GDV , Phelan JP , eds. Critical Care Obstetrics , 2nd edn. Boston : Blackwell Scientifi c , 1991 : 223 – 250 . 91 Caritis SN