SESSION TYPE: Critical Care Student/Resident Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Only a few cases of rhabdomyolysis in the setting of severe hyponatremia have been described in the literature. Rhabdomyolysis related to rapid correction of hyponatremia secondary to Psychogenic Polydipsia (PP) is rare 1. Extremely high creatinine phosphokinase (>200,000) has never been reported in this scenario. We report such a case.

CASE PRESENTATION:

A 39 y/o AAM with history of schizophrenia on Olanzapine presented with acute onset of generalized tonic-clonic seizure. Upon arrival to the ER, he was administered Lorazepam, Succinylcholine and intubated. CT scan of the head was normal. Serum sodium of 114, urine osmolality of 61 and serum osmolality of 245 suggested hyponatremia as the etiology. His mother confirmed suspicion of polydypsia. Vital signs were stable. Patient was afebrile. Patient was administered hypertonic saline and transferred to the MICU. Further labs revealed a CK of 4740. Urine was positive for myoglobunuria confirming rhabdomyolysis. Patient was quickly extubated and a physical examination was normal with no signs of muscle rigidity. As shown below, his Sodium started to rapidly correct and CK started to trend up to reach a peak of 214910. Hypotonic fluid infusion was initiated. Oral fluid intake was restricted. CK and renal function gradually improved over 10 days.

DISCUSSION:

Our patient had many risk factors for rhabdomyolysis including hyponatremic seizures, use of succinylcholine, and possible neuroleptic malignant syndrome due to antipschychotic medication. Rapidly uptrending CK in the absence of continued seizure activity along with lack of fever and muscle rigidity argued against the above possibilities. We found few case reports of rhabdomyolysis after correction of hyponatremia in PP 1-3, possibly complicated by atypical antipsychotics. But none of those reported CK levels as seen in our patient.

CONCLUSIONS:

There seems to be a synergistic relationship between atypical antipschychotic induced muscle membrane changes and rapid correction of hyponatremia leading to severe rhabdomyolysis. One should anticipate and monitor serum CK levels while taking care of PP induced hyponatremia for the early recognition and treatment of rhabdomyolysis in order to prevent renal failure.1) Rizzieri DA. Rhabdomyolysis after correction of hyponatremia due to psychogenic polydipsia. Mayo Clin Proc 1995;70:473-6.2) Wicki J, Rutschmann OT, Burri H, Vecchietti G, Desmeules J. Rhabdomyolysis after correction of hyponatremia due to psychogenic polydipsia possibly complicated by clozapine. Ann Pharmacother 1998;32:892-5.3) Zaidi AN. Rhabdomyolysis after correction of hyponatremia in psychogenic polydipsia possibly complicated by ziprasidone. Ann Pharmacother 2005;39:1726-31.DISCLOSURE: The following authors have nothing to disclose: Ibrahim Faruqi, Srikanth MukkeraNo Product/Research Disclosure InformationUniversity of Florida, Gainesville, FL.

SESSION TYPE: Infectious Disease Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Legionella pneumophila is a recognized cause of rhabdomyolysis. There are reports of severe rhabdomyolysis and subsequent kidney failure related to Legionella with significant mortality. We present a case of Legionella pneumonia in an alcoholic man who presented with severe rhabdomyolysis and acute renal failure who recovered successfully.

CASE PRESENTATION:

A 42-year-old alcoholic male presented with three days of fever, chills, productive cough with yellowish sputum and shortness of breath. He also complained of myalgia and watery non-bloody diarrhea. A few days prior to admission the patient had cleaned an air conditioning system in a restaurant. He had a 20-pack/year smoking history. On admission he was normotensive but tachycardic and febrile (102.1F); his oxygen saturation was 90% on two liters nasal cannula. He was diaphoretic with normal mental status. Scattered rales were auscultated in the right lower lobe. Laboratory studies revealed a leukocytosis with bandemia and thrombocytopenia. He was hyponatremic. His BUN was 24 and creatinine of 1.9. Lactic acid was normal. CPK was 19,086. The ABG revealed a metabolic acidosis. A chest X-ray show right upper lobe infiltrate. CT scan showed extensive consolidation of the right upper lobe and the superior segment of the right lower lobe. Legionella urine antigen was positive and levofloxacin and rifampin were started. The following day the patient developed respiratory distress and was intubated. A lorazepam drip was started for possible delirium tremens (DTs). His CPK initially decreased to a nadir of 7,450 on day 4, but subsequently increased to a maximum of 110,355 on day 8. He developed worsening renal failure that required hemodialysis on day 4. Daily fevers continued for more than 15 days despite antibiotic therapy. Chest x-ray showed significant improvement by day 12. Kidney function recovered completely and hemodialysis was discontinued. Patient was extubated on day 21. Muscle weakness persisted.

DISCUSSION:

Legionella is a known cause of pneumonia requiring ICU admission. Severe rhabdomyolysis leading to renal failure has been reported with Legionella Pneumonia. Mortality is high. We report a case of Legionella pneumonia associated with severe rhabdomyolysis (CPK level>100 000), renal failure, and protracted fevers despite appropriate antibiotic treatment. A possible confounding factor was our patient's history of alcohol abuse and possible DTs, which can be associated with rhabdomyolysis. However our patient's CPK level continued to rise despite the absence of clinical evidence of DTs. The patient survived after a prolonged ICU course.

CONCLUSIONS:

The current case illustrates the potential for severe rhabdomyolysis in patients with Legionella pneumonia as well as other confounding comorbidities.1) McConkey J, Obeis M, Valentini J, & Beeson MS. Legionella pneumonia presenting with rhabdomyolysis and acute renal failure: a case report. J Emerg Med 2006;30(4):389-392.DISCLOSURE: The following authors have nothing to disclose: Eduardo Andre, Craig Thurm, Javeria Bhawal, Kelly Cervellione, Kunal PatelNo Product/Research Disclosure InformationJamaica Hospital Medical Center, Jamaica, NY.

SESSION TYPE: Critical Care Student/Resident Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Etiologies for Status Epilepticus (SE) are broad, but encephalitis is a unique trigger for refractory SE. We present a case of HHV6 encephalitis in an immunocompetent male who developed severe refractory SE from HHV6B.

CASE PRESENTATION:

A previously healthy 21 year old male was admitted with signs of confusion and disorientation. The patient had had a febrile episode with some non-specific cervical lymphadenopathy that resolved with Augmentin. His history was benign, with no falls, trauma, exposures, travels, drug use or previous episodes. After admission, the patient developed status epilepticus that was not controlled with IV Valproate, Phenytoin, Levetiracetam, Lorazepam and Midazolam, and necessitated mechanical ventilation. Extensive CSF testing was negative, except for HHV6-type B PCR positivity. Admission MRI was normal but progressed to bilateral hippocampal enhancement and then hyperintense bihemispheric signal (without laminar necrosis). Clinically, the patient deteriorated in spite of optimal treatment; burst suppression was achieved with IV Pentobarbitol and IV Propofol with heroic doses of IV Midazolam (>100mg/hr), but relapsed when drug therapy was marginally deescalated. Repeat LP showed persistent HHV6B, which was treated with Ganciclovir and later Cidofovir along with IV Methylprednisone. The patient showed signs of vasomotor instability at day 21, in spite of vasopressor support, and at the family's wishes care was withdrawn.

DISCUSSION:

It has been published that HHV6 has known epileptogenic properties. This virus usually affects young patients with immunosuppression, but recently has been found in immunocompetent adults. The diagnosis is usually made via HHV6 (A/B) lab titers, given the fact that clinical presentation is highly variable. Imaging is not specific for this syndrome but bilateral hippocampal enhancement may offer an early clue to HHV6 encephalitis. Other MRI findings include increased mesial temporal lobe signal and cortical laminar necrosis. The current standards of care in encephalitis/ meningitis do not address the increasing incidence of a highly epileptogenic virus such as HHV6. As the seizures in HHV6 encephalitis are resistant to conventional treatment, a delayed diagnosis frequently leads to an often fatal, refractory SE.

CONCLUSIONS:

HHV6 should be sought early in immunocompetent adults with undiagnosed encephalitis and seizures, with Ganciclovir/Cidofovir and Methyprednisone added empirically along with aggressive management of seizures to prevent progression to catastrophic SE.1) Birnbaum et al. Severe meningoencephalitis caused by human herpesvirus 6 type B in an immunocompetent woman treated with ganciclovir. Clin Infect Dis. 2005 Mar 15;40(6):887-9.2) Provenzale et al. Extrahippocampal involvement in human herpesvirus 6 encephalitis depicted at MR imaging. Radiology. 2008 Dec;249(3):955-63.3) Theodore et al. Human herpes virus 6B: a possible role in epilepsy? Epilepsia. 2008 Nov;49(11):1828-37.DISCLOSURE: The following authors have nothing to disclose: Aaron Persinger, Amol Patil, Susanna Von EssenNo Product/Research Disclosure InformationUNMC, Omaha, NE.

SESSION TYPE: ARDS/Lung Injury PostersPRESENTED ON: Wednesday, October 24, 2012 at 01:30 PM - 02:30 PM

PURPOSE:

A subset of spontaneously breathing patients with adult respiratory distress syndrome (ARDS)/acute lung injury (ALI) achieves low tidal volume goals only when delta pressure is titrated downward to continuous positive airway pressure (CPAP). We performed a retrospective observational study to assess the safety of CPAP alone for invasively mechanically ventilated, spontaneously breathing patients with ARDS/ALI.

METHODS:

The records of all adult patients with respiratory failure and a PaO2/FiO2 (P/F) ratio < 300 who were invasively ventilated using CPAP at the University of Missouri Hospital between 8/1/2008 and 11/7/2009 were reviewed. Patients undergoing active weaning were excluded. Sedation requirements, respiratory rate and P/F ratio were compared in individual patients ventilated using CPAP versus conventional modes.

RESULTS:

23 patients were included (13 males and 10 females: age range of 19 to 78 years). The mean BMI was 36 kg/m2. The median time on CPAP was 51 hours. No difference was seen in the mean respiratory rate (18.8 vs. 18.78; p=0.99 ) or sedation requirements [propofol (15.0 vs. 19.5; p= 0.48), ativan (0.02 vs. 0.07; p= 0.54), versed(0.76 vs. 1.11; p= 0.41) or fentanyl(79.4 vs. 92.1; p= 0.54)] using CPAP vs. conventional modes respectively. P/F ratio was slightly better (183.80 vs 209.72; p=0.02) and survival was 87% (vs. 40-74% historical control) in the CPAP group.

CONCLUSIONS:

Invasive CPAP appears safe and well tolerated in spontaneously breathing patients with ARDS/ALI.

CLINICAL IMPLICATIONS:

Invasive CPAP may be a useful mode in patients with ARDS/ALI.DISCLOSURE: The following authors have nothing to disclose: Shilpa Patel, Casey Stahlheber, Troy Whitacre, Dexter Burns, Stevan WhittNo Product/Research Disclosure InformationUniversity of Missouri, Columbia, MO.

Although, neuropsychiatric morbidity is quite high in patients with systemic lupus erythematosus (SLE), catatonia has been rarely reported. We report a case of a 22-year-old female who presented with catatonic symptoms at the time of relapse of SLE and have discussed the presentation in the context of existing literature with regard to phenomenology of catatonia, psychiatric co-morbidity and treatment of catatonia in patients with SLE.

AIM:

To determine the frequency and clinical correlations of catatonia in older patients referred to a liaison psychiatry service in a general hospital.

PATIENTS AND METHODS:

All patients over 65 years referred to liaison psychiatry were screened for catatonic phenomena with the Bush-Francis Catatonia Screening Instrument (BFCSI) between January and May 2012. Their clinical characteristics and the outcome of treatment were recorded.

RESULTS:

One hundred and twelve patients over 65 years were referred. Ten (8.9%) met research diagnostic criteria for catatonia and 7 (6.3%) Diagnostic and Statistical Manual of Mental Disorders, 4th Edition criteria for catatonia. All patients presented with the inhibited variant and 5 to 12 catatonic signs. Three patients presented concomitant delirium. The etiology of catatonia was multifactorial, and complications and death were frequent (40% and 20%, respectively). Lorazepam achieved full resolution of catatonia in 50% of patients.

CONCLUSIONS:

Catatonia in older adults referred to liaison psychiatry in a general hospital is not infrequent and has a multifactorial etiology. The BFCSI is a simple and reliable instrument to detect catatonia in this population. Lorazepam seems to be an effective treatment.

Agitated behavior constitutes up to 10% of emergency psychiatric interventions. Pharmacological tranquilization is often used as a valid treatment for agitation but a strong evidence base does not underpin it. Available literature shows different recommendations, supported by research data, theoretical considerations, or clinical experience. Rapid tranquilization (RT) is mainly based on parenteral drug treatment and the few existing guidelines on this topic, when suggesting the use of first generation antipsychotics and benzodiazepines, include drugs with questionable tolerability profile such as chlorpromazine, haloperidol, midazolam, and lorazepam. In order to systematically evaluate safety concerns related to the adoption of such guidelines, we reviewed them independently from principal diagnosis while examining tolerability data for suggested treatments. There is a growing evidence about safety profile of second generation antipsychotics for RT but further controlled studies providing definitive data in this area are urgently needed.

Associations between large cavum septum pellucidum and functional psychosis disorders, especially schizophrenia, have been reported. We report a case of late-onset catatonia associated with enlarged CSP and cavum vergae. A 66-year-old woman was presented with altered mental status and stereotypic movement. She was initially treated with aripiprazole and lorazepam. After 4 weeks, she was treated with electroconvulsive therapy. By 10 treatments, echolalia vanished, and catatonic behavior was alleviated. Developmental anomalies in the midline structure may increase susceptibility to psychosis, even in the elderly.

In the view of diverse CNS modulating properties of Fumaria indica, present study was planned to evaluate its putative anxiolytic activity in behavioural models of rats, followed by elucidation of mechanism of observed activity through biochemical estimations.Effects of seven daily 100, 200 and 400 mg/kg oral doses of a Fumaria indica extract (FI) was compared with those of an acute oral dose (5 mg/kg) of lorazepam in a battery of rat models consisting of open-field, elevated plus and zero maze, social interaction, and novelty induced feeding tests.Dose dependant antianxiety effects of FI observed in all tests were qualitatively similar to those of the reference anxiolytic drug. Although FI treatments did not alter the concentrations of noradrenaline and serotonin in hippocampus and hypothalamus, concentrations of both these monoamines were dose dependently elevated in prefrontal cortex of FI treated animals. Flunitrazepam binding in brain frontal cortex was also elevated by the extract. Moreover, higher levels of brain expressions of the cytokines TNF-α, IL-1β, and IL-10 observed in animals with prior experience on elevated plus maze were almost completely reversed by the lowest dose of FI tested in the behavioral models.Taken together, these observations strongly suggest that FI is a functionally novel type of antianxiety agent, and that inhibition of cytokine expressions in the brain could be involved in its mode of action.

In 2011 we have diagnosed 9 anorectal malformations (MAR). This means 13.3 cases/10.000 NB versusu the estimated incidence of 2 cases/10.000 NB. This accumulation of defects can not be due to chance, so we have decided to focus on its research.The study included all the patients with anorrectal malformations born in 2011. In all of them we analyzed: geographic area, age and health status of parents, pregnancy, exposure to teratogens, especially lorazepam intake, sex, gestational age, weight at birth, exploration of the abdomen and perineum, birth defects associated, imaging studies performed, treatment and current situation.All patients came from our province, and maternal age is under 20 years in 2 patientes and older than 30 in 7; male-dominated (8/1); low forms in 4 of 9 patients. 100% of newborns have some type of associated malformation, in genitals, urinary system or costovertebral. Clinical assessment and imaging study provided the right diagnosis in all the cases. It must be noted the absence of difficulties in the surgery treatment and a favorable outcome in all children.To this accumulation of cases with anorrectal malformation cases it is added a male predominanced, and a high incidence of associatedmalformations and high defects. We have not found an epidemiological explanation for this concentration of patients with anorrectal malformations. This forces us to continue our investigation if detected for some reason, currently not known.