80	M.G. Jeschke

6.3.3Lung

Pulmonary complications in the early phase are pulmonary edema and inhalation injury that was discussed above. A pulmonary problem that occurs during ICU or hospital stay is VAP (ventilation-associated pneumonia) and ARDS.

6.3.3.1 Ventilator-Associated Pneumonia

The ABA guidelines for prevention, diagnosis, and treatment of ventilator-associ- ated pneumonia (VAP) in burn patients were published in 2009 [15, 33]. The guidelines are as follows:

¥Mechanically ventilated burn patients are at high risk for developing VAP, with the presence of inhalation injury as a unique risk factor in this patient group.

¥VAP prevention strategies should be used in mechanically ventilated burn patients.

¥Clinical diagnosis of VAP can be challenging in mechanically ventilated burn patients where systemic inßammation and acute lung injury are prevalent. Therefore, a quantitative strategy, when available, is the preferable method to conÞrm the diagnosis of VAP.

¥An 8-day course of targeted antibiotic therapy is generally sufÞcient to treat VAP; however, resistant Staphylococcus aureus and gram-negative bacilli may require longer treatment duration.

¥Any effort should be made to reduce length of intubation.

Our policy is to administer antibiotics according to the length of hospitalization.

Patients admitted within the past 5 days should be started on an empiric regimen of Ceftriaxone 1 g iv q24h +/− cloxacillin 1Ð2 g iv q4Ð6 h

Penicillin Allergy:

Levoßoxacin 750 mg iv/po q24h Late Phase (admitted >5 days):

Piperacillin/tazobactam 4.5 g iv q6h (renal dosing required)

+/− vancomycin 1 g iv q12h (with preand post-levels around the third dose) Penicillin Allergy:

Tobramycin 2 mg/kg q8h (in nonobese patients with crcl >70 ml/min) + vancomycin 1 g iv q12h (with preand post-levels around the third dose)

Or

Meropenem 500 mg iv q6h (renal dosing required)

6.3.4Liver/GI

Severe burn injury causes numerous metabolic alterations, including hyperglycemia, lipolysis, and protein catabolism [3, 6, 34]. These changes can induce multiorgan failure and sepsis leading to signiÞcant morbidity and mortality [34Ð 36]. Liver plays a signiÞcant role in mediating survival and recovery of burn patients, and preexisting liver disease is directly associated with adverse clinical outcomes following burn injury [37Ð39]. In the study by Price et al. in 2007, they

6 Critical Care of Burn Victims Including Inhalation Injury	81

demonstrated that preexisting liver disease increased mortality risk from 6 to 27 %, indicating that liver impairment worsens the prognosis in patients with thermal injury. Severe burn also directly induces hepatic dysfunction and damage, delaying recovery. More recently, work by Jeschke et al. (2009) and Song et al. (2009) has shed light on the mechanism of the hepatic dysfunction following thermal injury, mainly by the upregulation of the ER stress response, and increased cell death contributing to compromised hepatic function postburn [40Ð45]. Thus, one must not only be cognizant of the signiÞcant deleterious effects of hepatic dysfunction in the thermally injured patient as it has signiÞcant consequence in terms of multiorgan failure, morbidity, and subsequent mortality of these patients but also focus on therapeutic modalities to alter this response and possibly improve outcome.

6.3.4.1 GI Complications/GI Prophylaxis/Enteral Nutrition

The effect of thermal injury on the gastrointestinal system was identiÞed in 1970 by Dr Basal Pruitt with the description of CurlingÕs ulcer. During the initial hours, splanchnic blood ßow is reduced, except for ßow to the adrenals and to the liver. Poorly perfused organs shift toward anaerobic metabolism leading to acidosis. Adequate ßuid resuscitation restores perfusion to a great extent. But with overenthusiastic ßuid delivery, increasing intra-abdominal pressures and consequently abdominal compartment syndrome (ACS) becomes a matter of concern in both adult and pediatric burn patients [19, 46]. The Ivy index (250 ml/kg ßuid resuscitation) is a cutoff value beyond which trouble is nearly certain. Abdominal pressures start rising, soon reaching the Ògray zoneÓ of 15Ð20 mmHg, and then the danger zone >20 mmHg, beyond which medical measures must be taken to reduce the IAP to avoid splanchnic organ ischemia. IAP monitoring is essential for TBSA >30 %. Abdominal compartment syndrome is a complication that is associated with high mortality, and in general, laparotomy should be avoided. Abdominal pressure should be controlled by diuresis, sedation, and even paralytics if needed. If the abdomen is burned checkerboard, escharotomies need to be performed.

The gut is extremely vulnerable to changes in perfusion and nutrition. Even short ischemia can lead to gut atrophy associated with several complications. Early enteral feeding should be initiated no later than 12 h after injury. The beneÞts of this strategy are numerous: increasing blood ßow to the splanchnic compartment before edema makes it impossible, maintaining pyloric function, maintaining intestinal motility, and reducing signiÞcantly infectious complications. Current recommendations are to place a nasogastric feeding tube as well as post-pyloric feeding tube.

During the initial phase postburn as well as after each ischemia-reperfusion hit, gastrointestinal function, including pyloric function, is vastly depressed. A true paralytic ileus will ensue for many days if the gastrointestinal tract is not used. Opiates and sedatives further depress the gastrointestinal function, and constipation is frequent and may become critical with the development of ileus and intestinal obstruction by feces. Prevention should be initiated from admission using Þbercontaining enteral diets, lactulose (osmotic cathartic), and enemas when the other measures have failed. Regular bowel movements need to be diligently monitored.