POSTERIOR REVERSIBLE ENCEPHALOPATHY SYNDROME IN A TRAUMA PATIENT WITH MULTIPLE GUNSHOT WOUNDS

Introduction/Background Posterior Reversible Encephalopathy Syndrome (PRES) is a neurological condition with variable manifestations confirmed by radiological findings of vasogenic edema. While the exact pathophysiology of the condition is unknown, the leading endothelial dysfunction theory posits that damage to the blood-brain-barrier due to hypertension, acute fluctuations in blood pressures, or toxin-mediated endothelial damage causes leak of vessel contents into the interstitial space.1 Clinicians may not be aware of trauma as an inciting factor for PRES given the scarcity of such cases in the literature. As such, we aim to increase recognition of these cases in clinical practice. Here we delineate the first reported case of PRES occurring in a trauma patient with multiple gunshot wounds (GSW). Case Presentation A 24-year-old male with a history of colostomy after GSW to the abdomen and without history of hypertension presented to the trauma bay with multiple GSW to the abdomen, chest, and left thigh. On evaluation, the patient was tachycardic but normotensive, and the FAST exam was positive for a right pleural effusion. An exploratory laparotomy was performed with diaphragm and liver laceration repair, pericardial window, and chest tube placement bilaterally. He received 4 units of packed red blood cells, 4 units of fresh frozen plasma, and 1 unit of platelets during the case. An ABThera was placed, and the patient was taken back to the OR the next day for reexploration, abdominal washout, and abdominal fascial closure. He was extubated on hospital day 2, at which point the primary medicine team noted the patient was agitated and confused. He was initially managed on haloperidol, and later quetiapine was added. On hospital day 9, a non-contrast CT of the head was obtained for persistent altered mental status which was suggestive of multifocal acute infarcts. Followup magnetic resonance imaging (MRI) was performed and demonstrated small acute infarcts in the right frontal and left posterior occipital lobe, as well as T1 hypointensity, and T2 hyperintensity with associated FLAIR signal in the bilateral posterior horns of the occipital lobes consistent with PRES (Fig. 1). Neurology was consulted regarding the infarcts on imaging and for new onset memory deficits, somnolence, and agitation. On the initial neurological exam, the patient was alert and oriented, and the only defects found were difficulty with concentration and calculation. On hospital day 11, the patient was no longer oriented to the month and did not know the current or first president. He registered 3/3 words but recalled 0/3 words, and his language was mildly slowed compared to the previous day. The patient also demonstrated cognitive impairment in concentration and calculation. On hospital day 12, he was drowsy but once again oriented to the month. New deficits found included decreased confrontation in upper visual fields bilaterally. The remainder of the neurological examination was normal. Repeat imaging reconfirmed suspicions for PRES, and a lumbar puncture was performed to rule out infection and was normal. Throughout his hospital course, the patient did not have seizures or headaches. He was started on aspirin and worked with PT/OT to regain strength throughout his hospital stay. Other postoperative complications included a postoperative fever on hospital day 4. Blood cultures were obtained and grew Bacteroides vulgatus and a Clostridium species, for which he was treated with IV piperacillin-tazobactam. He also had an infected biloma, found on CT angiogram of the abdomen and pelvis that was obtained for abdominal pain with new tachycardia on hospital day 8. A drain was placed and ERCP with stent placement was performed. Culture from the drain grew Pseudomonas aeruginosa and Enterococcus faecalis, which was treated with outpatient antibiotics.The patient was discharged on hospital day 16 with an appropriate pain regimen, amoxicillin-clavulanate and levofloxacin for his infections, and instructions to return for stent removal in 8 weeks and repeat MRI in 1-2 months to evaluate for resolution of PRES. At the time of discharge, his mental status remained altered as described above. The patient was lost to follow-up, thus no MRI was performed after discharge and there were no outpatient appointments made. Discussion The clinical manifestations of PRES are variable. While the most common presentation is seizures; encephalopathy, altered mental status, headache, and changes in vision can also occur.2 The etiology of PRES is multifaceted. Hypertension and blood pressure fluctuations are the most commonly reported precipitating cause of the condition, with immune-suppressing medication, infection, and preeclampsia being reported less commonly.2 In the majority of the cases implicating blood pressure, the mechanism of PRES is hyperperfusion overwhelming the capacity of cerebral autoregulation leading to extravasation of fluid and vasogenic edema.1 In cases without hypertension as a precipitating factor, a cytotoxic theory has been proposed with endogenous and/or exogenous toxins damaging endothelial cells of the blood-brain-barrier. This leads to release of vasoactive compounds from endothelium causing vascular leakage.1 Common etiologies of PRES that likely arise from the cytotoxic mechanism include immunosuppressant use, infection, (pre)eclampsia, and renal failure. Blood transfusion has been reported in previous case studies as a rare cause of PRES, with recent literature reviews identifying less than 30 reported cases.3 The posited mechanism of this etiology is a sudden increase in blood viscosity due to rising hematocrit levels, causing injury to endothelium, similar to the cytotoxic theory of PRES.4The significance of the above etiologies of PRES is that these phenomena (blood pressure changes with hypertension, infection leading to sepsis, and blood transfusions) are complications which may arise in the course of treatment in patients with acute trauma from external injury. However, this concept has been poorly defined. In order to further explore the possible link between acute trauma and its complications with PRES, we aim to provide a brief overview of the current literature regarding PRES following acute trauma from external injury. The general demographics of our final population of twelve patients are listed in Table 1 below. The most common trauma type related to eventual development of PRES was motor vehicle accidents (MVAs), accounting for eight of the twelve cases.5, 6, 9, 12,-14 MVAs included collisions of a motor vehicle with another object or vehicle, or collision with a motor vehicle as a pedestrian. The remainder of causes in other cases were composed of falls (2) or other blunt trauma (2).7, 8, 10, 11 Blood pressure abnormalities were present in all but one case of PRES related to external traumas.5-10, 12-14 Hypertension and blood pressure fluctuations are well established causes of PRES, making up the most commonly reported precipitating cause of the condition; this aligns with our findings. Three of the twelve cases also involved transfusions in the acute setting after a trauma, and two of the twelve cases developed sepsis during the course of their hospital stay, which may have contributed to the development of PRES.5, 6, 8, 10 Other potential factors known to be related to PRES that were found within the literature review included renal dysfunction and cytotoxic medications.5, 8, 12Perhaps equally important are the symptomatic manifestations of PRES in patients in acute-trauma settings. Seven of the twelve cases mentioned seizures as a notable clinical occurrence, including both single generalized seizures and status epilepticus.5, 7-9, 12-14 Six patients experienced headaches and three experienced vision changes, although it is unclear if these are symptomatic manifestations of hypertension or related to development of PRES.6-9, 14 In terms of diagnostic imaging, MRIs (identified as the standard of care for PRES) were ordered on all patients, and the distribution of PRES-related imaging findings uniformly implicated the posterior circulation.2, 5-14 Some cases (5) had anterior circulation involvement in addition; however, in no cases was only the anterior circulation involved.5, 9, 10, 13, 14 Notably, all articles were written in the last decade, with the exception of one.5-8, 10-14 In the case study above, the patient's hospitalization included multiple potential causes of PRES. These included the large volume blood transfusion upon admission, blood pressure fluctuations, and infection. Recorded systolic blood pressures ranged from 94-163 mmHg, diastolic blood pressures ranged from 42-124 mmHg, and mean arterial pressure ranged from 70-137 mmHg. These same factors were found across the cases in the literature review, supporting the correlation between these complications of trauma and the future development of PRES. There is a scarcity of cases regarding the correlation between trauma and PRES in the literature, and there are none regarding gunshot wounds as the source of trauma preceding PRES. The cases discussed in the literature review all were precipitated by trauma; however, the case report we present above is the first reported case of PRES incited by a gunshot wound specifically. This case report aims to increase awareness of PRES as a possible complication of traumatic injuries and associated resuscitation measures. While rare, it is important to keep this diagnosis in mind as trauma patients frequently experience several inciting factors such as hemodynamic instability, blood transfusions, and infections. (Figure Presented).