Aggressive Intravenous Hydration Research Articles

Lessons on aggressive intravenous hydration in acute pancreatitis: A meta-analysis of clinical trials

Lessons on aggressive intravenous hydration in acute pancreatitis: A meta-analysis of clinical trials

Gastric Adenocarcinoma with Acute Tumor Lysis Syndrome: An Unusual Association

Purpose: Acute Tumor Lysis Syndrome (ATLS) is the constellation of symptoms, signs and abnormal laboratory findings caused by disintegration of tumor cells and subsequent release of their content in to blood. ATLS is primarily seen in cancers of blood but it has also been noted in solid tumors. Here we describe a very rare case of ATLS in a patient with gastric adenocarcinoma. A 51-year-old man came to our emergency room with complaint of generalized weakness, severe nausea and vomiting for 2 days. He also complained of decreased urination. He was diagnosed with infiltrating adenocarcinoma of stomach about 9 months ago. Since then, patient was receiving chemotherapy with cisplatin, docetaxel and 5-fluorouracil. His last chemotherapy was about 2 months before this admission. Physical examination was reveled mild epigastric tenderness and sluggish bowel sounds. Pertinent laboratory findings are summarized in the table. Gastric outlet obstruction was ruled out by history and physical examination. These laboratory findings were highly suggestive of ATLS. Treatment with aggressive intravenous hydration and allopurinol was started. A CT scan of abdomen revealed multiple enlarged mesenteric lymph nodes, gastric and colonic wall thickening, and multiple metastatic lesions in liver and adrenals which were suggestive large tumor burden. Patient was started on renal replacement therapy and after 2 hemodialysis sessions, patient's renal functions began to improve. Later patient responded well to symptomatic treatment with improvement in her general condition and complete resolution of electrolyte imbalance in 8 days. Association of gastric carcinoma and ATLS is very rare. This case illustrates the need for increased vigilance for ATLS even in solid tumors. An accurate diagnosis of ATLS is very essential in solid tumors as mortality in these patients is about 35% (1). We suggest that ATLS should be suspected in patients with acute renal failure accompanied by hyperuricemia.Table: Laboratory findings at the time of admission

Lessons From Clinical Trials on Early Aggressive Intravenous Hydration in Acute Pancreatitis: A Meta-analysis: Presidential Poster

Purpose: Despite limited clinical research in humans, guidelines have uniformly stated that early aggressive intravenous hydration (EAIH) is an important part of the management in patients with acute pancreatitis (AP). Recent clinical studies evaluating the efficacy of EAIH have demonstrated conflicting results. The purpose of our study was to systematically review, analyze and combine the different studies in a meta-analysis in order to determine the efficacy of EAIH in the management in patients with AP. Methods: A systematic search of the literature was performed to identify clinical trials evaluating the role of EAIH in patients with AP. In order to be included in the analysis, the published study needed to include patients with AP enrolled in a consecutive, prospective or retrospective fashion; provide information regarding gender, etiology, amount of fluid for each group, outcome such as organ failure, necrosis, and/or mortality, and the amount of fluid provided over the initial 24-72 hours. When combining the various studies, the weighted mean of power (sample size) was used to determine the relative value of significance. Sensitivity analysis evaluated study design, inclusion criteria, timing, type of fluids and severity of patients included. Results: Nine published studies fulfilled the criteria to be included in the analysis, which included 1,179 patients: 668 patients in the EAIH group, 511 patients in the control group. The volume of fluid provided over time differed considerably. However, when combining the studies, the EAIH group received 4,325 ± 2,322 cc during the first 24 hours and the control group received 2,643 ± 2,822 cc during the first 24 hours. There were no significant differences in the age, gender, and etiology distribution among the studies (p>0.05). There was no significant difference in the development of organ failure, pancreatic necrosis, morbidity or mortality (p>0.05). However, in a subgroup analysis (sensitivity analysis), there was a decrease in morbidity and mortality when the hydration was provided more aggressively during the first 6-12 hours (p=0.02). In addition, when excluding studies that only included patients with severe disease, there was a significant reduction in morbidity in patients undergoing EAIH during the first 24 hours (p=0.03). Conclusion: EAIH appears to be most beneficial in preventing morbidity and mortality when applied to patients with AP early in the course of the disease, within the first 6-24 hours. There does not appear to be a benefit to aggressive hydration in patients with AP beyond the first 24 hours. The benefit of EAIH appears to be in patients with mild disease, preventing the development of organ failure and/or pancreatic necrosis.

Tratamiento de las urgencias del metabolismo fosfocálcico

The treatment of phospho-calcium metabolism emergencies will depend on different aspects such as the severity of the ion alteration, the precipitating cause, associated signs and symptoms and presence of other accompany hydroelectrolytic disorders. In every case, the vital signs and diuresis should be monitored periodically, performing an electrocardiogram and basic biochemistry study (that includes creatinine, sodium calcium, phosphorus) and venous, basal blood gases study periodically to monitor response to treatment.In the cases of hyperkalemia, aggressive intravenous hydration serum therapy is essential, adding, if necessary, loop diuretics and other drugs (bisphosphonates, corticosteroids, calcitonin, etc.) or hemodialysis.Treatment of hypokalcemia basically consists in calcium supplementation, orally if possible (in cases with mild symptoms) or intravenously. If there is no improvement after 24 hours of treatment, concomitant administration of magnesium supplements should be considered.Hyperphosphatemia should be treated with intravenous hydration, closely monitoring the serum calcium levels (due to risk of appearance or exacerbation of hypokalcemia), using hemodialysis, in severe cases, or in those accompanied by renal failure.Severe hypophosphemia (serum phosphorus <1mg/dl) generally requires intravenous parenteral supplementation, close monitoring of the rest of the ions being especially important due to the risk of the appearance of other hydroelectrolytic alterations.

Hypercalcemic crisis induced by calcium carbonate.

We report a rare case of drug-induced hypercalcemic crisis in an elderly male resulting from calcium-containing supplements facilitated by thiazide diuretic and angiotensin-converting enzyme inhibitor. A 61-year-old male presented with hypercalcemic crisis along with renal insufficiency and metabolic alkalosis, mimicking the ‘calcium-alkali syndrome’. The patient responded to aggressive intravenous hydration along with emergent hemodialysis and salmon calcitonin. He did not have hyperparathyroidism or malignancy. History revealed an average daily intake of only 1200 mg of calcium carbonate along with vitamin D 1000 U/day over an extended period of time. The patient completely recovered in 3 days and had normal serum calcium, parathyroid hormone and phosphorous level at 3-month follow-up. The case highlights the life-threatening perils of indiscriminate and often excessive intake of calcium-containing supplements in an appropriate clinical setting. We also briefly discuss the epidemiology, clinical and laboratory features along with the recent advances in the understanding of the pathophysiology of calcium-alkali syndrome.

Oncologic emergencies

To provide an up-to-date review of current literature on the pathophysiology, diagnosis, and management of five key malignancy-related complications: superior vena cava syndrome, malignant pericardial effusion, malignant spinal cord compression, hypercalcemia, and acute tumor lysis syndrome. Database searches and review of relevant medical literature. Malignancy-related complications demand increased attention from intensivists due to their frequency and increasing cancer prevalence. Although such complications portend a poor prognosis, proper acute management can improve short-term outcomes by facilitating either definitive care of the underlying malignancy or the institution of appropriate palliative measures. Knowledge of malignancy-induced complications in critically ill patients expedites the ability of the intensivist to properly manage them. Five complications commonly requiring emergency management are addressed in this review. Specifically, superior vena cava syndrome may warrant radiation, chemotherapy, vascular stenting, or surgical resection. Malignant pericardial effusion may require emergency pericardiocentesis if cardiac tamponade develops. Malignant spinal cord compression demands immediate spinal imaging, glucocorticoids, and either surgery or radiation. Hypercalcemia requires aggressive intravenous hydration and a bisphosphonate. Acute tumor lysis syndrome necessitates intravenous hydration, rasburicase, and management of associated electrolyte abnormalities.

Calcium Abnormalities in Hospitalized Patients

Depending upon the method of measurement, hypocalcemia occurs in 15% to 88% and hypercalcemia occurs in 15% of hospitalized patients. Ionized calcium should be measured in place of total serum calcium to avoid errors related to hypoalbuminemia, which is seen commonly in acutely ill patients. Symptomatic hypocalcemia requires prompt intravenous calcium administration. Symptomatic hypercalcemia (most often caused by hyperparathyroidism or malignancy) warrants aggressive intravenous hydration to correct volume depletion and, usually, additional therapy with diuretics, bisphosphonates, calcitonin, or corticosteroids. Identification and treatment of the underlying cause of the calcium derangement must be addressed after the acute electrolyte abnormality is stabilized.

Adderall® Induced Acute Liver Injury: A Rare Cause

Purpose: Introduction: Toxin induced liver injury contributes to 30% of acute liver injury. Amphetamines and their derivatives are among the rarer causes of drug induced liver injury. Although both amphetamine and dextroamphetamine have been reported to individually cause liver injury, to our knowledge, Adderall®, a combination of both dextroamphetamine and amphetamine has not been associated with liver injury. We report a case of Adderall induced acute liver injury. To our knowledge this is the first case reported in the English medical literature. Case report: A 55 y.o. African American female presented with a 3 day history of malaise, anorexia, nausea, vomiting, and jaundice. The patient had a history of partial hepatic resection secondary to liver metastasis from colon cancer in 2006. She had been in remission since that time. She denied any risk factors for acute liver injury including complementary and alternative medications. She had been on Adderall XR 30mg twice a day for 11 months. The patient developed encephalopathy with worsening of liver enzymes and acute kidney injury by the second hospital day. In 72hrs, the patient's encephalopathy improved with lactulose. Renal function responded to aggressive intravenous hydration. The patient was discharged on the seventh hospital day with normal liver and kidney function. We arrived at a diagnosis of Adderall induced acute liver injury after excluding common etiologies of acute hepatic failure. Discussion: Amphetamine and its derivatives causing liver injury have been mentioned in the literature. Since amphetamines are rare causes of acute liver injury, physicians should first exclude common etiologies of acute hepatic failure. However, drug induced acute liver failure is considered to have a worse prognosis than viral causes of liver injury. Patients should be considered for emergency liver transplantation on an individual basis if conservative measures fail. However, data on the survival rate after liver transplantation in amphetamine induced fulminant hepatic failure is limited. Conclusion: Although few cases of amphetamine induced acute liver injury have been reported in the medical literature, no case of Adderall induced acute liver injury has been reported to our knowledge. In our patient, hepatic resection may have resulted in compromised functional reserve which, in turn, might have aggravated the Adderall induced hepatic insult. Meticulous supportive care was crucial for our patient with compromised liver function. Our case suggests that amphetamine like medications might need to be used with caution in patients with compromised liver function. Clinicians need to be alert to possible liver injury when using Adderall.

A 10-year-old boy with dark urine and acute kidney injury: question

A previously healthy 10-year-old boy presented to the Pediatric Emergency Unit during the winter with fever, myalgias, and muscular weakness since the previous day. The urine had turned a dark-brown color. The patient also had diarrhea and occasional vomiting for 2 days. The parents explained that a total dose of 2.1 g of ibuprofen (i.e., 60 mg/kg) had been administered as self-medication the day before. Upon admission, the patient’s blood pressure was 113/ 78 mmHg, and his heart rate was 123/min. Axillary temperature was 39.5°C. Physical examination showed muscular weakness in both legs and flank tenderness. The findings of the respiratory, cardiac, and neurological examinations were normal. The test results on admission were as follows: rapid testing for Influenza A was positive; urine dipstick was positive for bilirubin (3+), blood (3+), and protein (3+). Laboratory tests showed a creatine kinase level of 318,000 U/l, urea nitrogen 18 mmol/l, creatinine 214 μmol/l, bicarbonate 16 mmol/l, and potassium 5 mmol/l. A diagnosis of massive rhabdomyolysis with acute kidney injury (AKI) was made. Rhabdomyolysis progressed with a peak creatine kinase level of 348,000 U/l, lactate dehydrogenase 124,000 U/l, serum myoglobin 42,873 μg/l, aspartate aminotransferase 7,122 IU/l, alanine aminotransferase 1,462 IU/l, metabolic acidosis, hyperkalemia of 5.2 mmol/l, hypocalcemia of 1.5 mmol/l, and hyperphosphoremia of 2.7 mmol/l. Ultrasound imaging showed enlarged kidneys with a loss of corticomedular differentiation. Despite aggressive intravenous hydration with normal saline and urine alkalinization with sodium bicarbonate, urinary output decreased, and the patient developed anuric renal failure on day 2 with a creatinine level of 663 μmol/l and urea nitrogen level of 35 mmol/l. Hemodialysis was initiated on day 2. Nine hemodialysis sessions were necessary until day 16. The patient had no cardiac complication. His condition improved, with diuresis The answer to this question can be found at doi:10.1007/s00467-0111767-3.

Decreased Mortality in Acute Pancreatitis Related to Early Aggressive Hydration

Early aggressive intravenous hydration is believed to prevent morbidity and mortality by preventing intravascular volume depletion and maintaining perfusion of the pancreas possibly preventing pancreatic necrosis. The following study was initiated to determine the relationship between the observed decrease in mortality and the role of early aggressive hydration. A consecutive series of patients with acute pancreatitis from a single community hospital in 1998 were compared to a consecutive series of patients with acute pancreatitis from the same institution in 2008. Significantly more patients developed pancreatic necrosis; 26 (15%) of 173 patients in 1998 compared to 4 (4%) of 113 patients in 2008. The mean rate of hydration was significantly higher in 2008 compared with that in 1998 (P = 0.02). In 1998, hydration was provided at 184 mL/h during the first 6 hours and 188 mL/h during the first 12 hours compared with 284 mL/h during the first 6 hours and 221 mL/h during the first 12 hours in 2008. There was a significant decrease in mortality in 2008 compared with that in 1998 (3.5% vs 12%, P = 0.03). The decrease in mortality seen in patients with acute pancreatitis during the last decade may be related to the increased aggressive hydration preventing pancreatic necrosis.

Combined Amifostine And Cryotherapy For Prevention Of Oral Mucositis (OM) Following High Dose Chemotherapy With Melphalan And Autologous Hematopoietic Cell Transplant (HCT) For Multiple Myeloma (MM)

OM is a major cause of morbidity following autologous HCT for MM. Amifostine is a free radical scavenger that reduces proinflammatory cytokine production. Cryotherapy causes vasoconstriction of vessels in the oral cavity. Randomized controlled trials have demonstrated a significant reduction in the severity and duration of OM when amifostine or cryotherapy is administered with high dose melphalan prior autologous HCT for MM. To date, no report has been made of outcomes when both treatments are used concurrently. We performed 28 autologous HCTs on 21 patients with MM in an outpatient setting. Patients received amifostine 740 mg/m2 24 hours prior to and immediately prior to melphalan (200 mg/m2 for 19 patients and 140 mg/m2 for 2 patients; dose dependent on renal function). Cryotherapy was administered for four hours beginning 30 minutes prior to the administration of melphalan. Six patients had a decline in systolic blood pressure of≥20% of baseline following the administration of amifostine. Aggressive intravenous hydration and Trendeleberg positioning resulted in the rapid return to baseline blood pressure in all cases. Prehydration and holding antihypertensive medications for 24 hours prior to the first dose of amifostine reduced symptomatic hypotension. No patient was admitted for OM. The one patient who required both total parenteral nutrition and narcotic analgesics for grade III OM did not remove his dentures during cryotherapy. One patient experienced grade II OM that was managed with oral narcotic analgesics. The remaining 19 patients experiencing either grade I (n=1) or no (n=18) OM. Combined amifostine and cryotherapy is a well-tolerated and effective method of reducing OM following high dose melphalan and autologous HCT for MM.

Cisplatin Overdose

Cisplatin is one of the most widely used antineoplastic agents in the treatment of solid tumour and haematological malignancies, including cancers of the testes, ovary, bladder, head and neck, oesophagus, stomach and lung, as well as lymphoma and osteosarcoma. Its non-specific targeting commonly results in adverse effects and toxicities affecting the gastrointestinal, renal, neurological and haematological systems even when administered at standard doses. Since cisplatin-related toxicities are dose-dependent, these may be more pronounced in the setting of a cisplatin overdose, resulting in significant morbidity and/or mortality. The incidence of cisplatin overdoses is unknown; however, early-phase clinical trials utilizing high-dose cisplatin, and case reports in the overdose setting have characterized the clinical features associated with cisplatin overdoses, highlighting some therapeutic strategies for consideration. To date, no published guidelines exist for managing a cisplatin overdose. The major toxicities of a cisplatin overdose include nausea and vomiting, renal insufficiency, electrolyte abnormalities, myelosuppression, ototoxicity, peripheral neuropathy, hepatotoxicity and retinopathy. Diarrhoea, pancreatitis, seizures and respiratory failure have also been reported. No specific antidote for cisplatin exists. Key management principles and strategies to lessen toxicities include renoprotection and enhancing drug elimination with aggressive intravenous hydration with or without the use of an osmotic diuretic, and avoidance of nephrotoxic medications. Sodium thiosulfate and plasmapheresis, with or without haemodialysis support, should be strongly considered. Close monitoring of clinical and laboratory parameters, and institution of supportive therapies, including antiemetics and haematopoietic colony stimulating factor support, are warranted. Based on the current literature, experimental therapies such as amifostine, ditiocarb sodium (diethyldithiocarbamate), acetylcysteine, fosfomycin and colestipol are of limited clinical effectiveness and remain investigational. This review serves to highlight the clinical spectrum of toxicities resulting from a cisplatin overdose, to critically appraise the available literature and to present a suggested algorithmic approach for the initial management of a cisplatin overdose.

Bacille Calmette-Guérin (BCG) Immunotherapy-Induced Celiac Crisis: A First Manifestation of Silent Celiac Disease in an Elderly Patient

Purpose: Introduction: Celiac disease (CD) is an immune-mediated glutensensitive enteropathy with various clinical presentations. BCG, in addition to its role as a vaccine against tuberculosis, has been used as an immunotherapeutic agent in patients with bladder cancer by intravesical instillation. We present an elderly patient with new onset of celiac disease after intravesical treatment with BCG, the first such report to our knowledge. Case Report: An 81-year-old woman with recently diagnosed superficial bladder cancer, treated with resection and intravesical BCG instillation, was seen because of multiple episodes of spurious non-bloody diarrhea for 3 days associated with colicky abdominal pain, nausea and non-bilious vomiting with no fever. On arrival, she was hypotensive requiring aggressive intravenous hydration. Physical examination was otherwise unremarkable. Similar episodes occurred twice 3 months ago, 2 weeks after her fourth BCG dose, requiring hospitalization and fluid resuscitation. At that time she was treated empirically for Clostridium difficile colitis and discharged without any definitive diagnosis. This admission, work up revealed normocytic anemia, +fecal WBC, and negative findings for C. difficile toxin and stool culture tests for cryptosporidia and ova and parasites. CT scan of the abdomen was unremarkable. Tissue transglutaminase antibody and gliadin IgG were mildly elevated. Endoscopy-guided small intestinal biopsy showed typical pathological characteristics of CD. The patient responded to a gluten-free diet with marked improvement in her symptoms. The diagnosis of latent CD was subsequently reconfirmed by genetic analysis. Discussion: The exact mechanism of BCG action is unknown, but intravesical instillation triggers a variety of local immune responses including stimulation of CD4 T cells, macrophages, cytokines and IFN-γ resulting in tumor destruction. The systemic response to intravesical BCG instillation has not been studied and has been thought to have only local effect. However, rare cases of BCG-induced HLA B27-positive arthritis have been reported. We propose that this new emergence of latent CD shortly after BCG therapy in our elderly patient is not just a coincidence. The impact of systemic immune response and possibly new onset of autoimmune disorders, such as CD, with intravesical BCG needs to be investigated. Clinicians should consider the diagnosis of activated CD (perhaps including other inflammatory bowel diseases) in patients with a new onset of unexplainable diarrhea after BCG therapy. More studies will need to be done to further validate this relationship, which suggests wider risks of activating remote immune reactions with BCG.

Sunitinib‐Related Fulminant Hepatic Failure: Case Report and Review of the Literature

Drug-induced hepatotoxicity is an infrequent but life-threatening complication. Sunitinib is a multitargeted receptor tyrosine kinase inhibitor approved for treatment of renal cell carcinoma and gastrointestinal stromal tumor. However, results from preapproval clinical trials suggest an equivocal hepatic risk profile for sunitinib. We describe a 75-year-old woman with renal cell carcinoma who was admitted to the intensive care unit after experiencing fulminant hepatic failure during sunitinib therapy. The patient's hepatic and renal chemistries had been within normal limits throughout four previous cycles of sunitinib therapy spanning 9 months. After the fifth cycle, she complained of a 3-day history of severe diarrhea and dehydration. Her abnormal laboratory test results included the following: total bilirubin level 5.9 mg/dl, aspartate aminotransferase level 3872 U/L, alanine aminotransferase level 3332 U/L, ammonia level 897 microg/dl, and an international normalized ratio of 4.8. Use of the Naranjo adverse drug reaction probability scale indicated a possible relationship between sunitinib and hepatotoxicity. Supportive care including aggressive intravenous hydration and reversal of coagulopathy was successful. The patient was discharged home on hospital day 7 without apparent longstanding sequelae. Clinicians should be aware of this possible adverse effect of sunitinib, and continued pharmacovigilance is imperative to accurately quantify the possible risk of sunitinib-related hepatotoxicity.

A Case of Occult Compartment Syndrome and Nonresolving Rhabdomyolysis

A 32-year-old African male presented with 10 hours of severe back pain. Initial computed tomography scan of the back showed no abnormality, and initial laboratory investigations were consistent with rhabdomyolysis. Despite stopping potential causative medications, aggressive intravenous hydration, and urine alkalinization, his creatinine kinase continued to steadily climb. Thirty-six hours after admission, a magnetic resonance imaging of his back was done because of new swelling over the right paraspinal muscles and loss of sensation in this region. Marked swelling of the right erector spinae muscles was observed, and right and left compartment pressure measurements were 108 and 21 mm Hg, respectively. He had urgent fasciotomy after which his rhabdomyolysis and pain recovered. Our case highlights the need for early consideration of compartment syndrome as a possible cause of back pain in the setting of rhabdomyolysis. Rhabdomyolysis can present in the absence of late complications such as neurological and vascular compromise.

Neuroleptic malignant syndrome variant in a patient receiving donepezil and olanzapine

A 78-year-old man with a 22-year history of schizoaffective disorder and a 5-year history of dementia presented to the emergency department with a 5-day history of fatigue, progressive weakness, confusion and lethargy, and a 1-day history of severe muscle stiffness. For the past 10 years the patient had been treated with olanzapine for an unspecified psychiatric illness, without adverse effects. One week before presentation the patient was started on donepezil to treat mild dementia. Physical examination, serum and urine laboratory evaluation, lumbar puncture, brain CT scan, brain MRI, electroencephalogram, chest X-ray, and electrocardiogram. A variant of neuroleptic malignant syndrome secondary to drug interaction. Discontinuation of donepezil and olanzapine, aggressive intravenous hydration, intravenous dantrolene, and bromocriptine via a nasogastric tube. The patient was also administered intravenous antibiotics for aspiration pneumonia, and carbidopa-levodopa for residual parkinsonian features.

Index of Suspicion

Index of Suspicion

STAPHYLOCOCCAL SCALDED SKIN SYNDROME: A RARE COMPLICATION OF A COMMON PATHOGEN.

Introduction Staphylococcal scalded skin syndrome (SSSS) is caused by an exfoliative toxin-producing strain of Staphylococcus aureus (SA). It is a disorder that is commonly seen in children but rarely found in adults. In recent years, there appears to be an increasing awareness of the diagnostic criteria, and as a result, there are now over 50 documented adult cases reported in the literature. However, only two adult cases have been documented from methicillin-resistant SA (MRSA). This is the first reported case involving communtiy-acquired MRSA meningitis in association with SSSS. Case Report A 45-year-old female with type 2 diabetes mellitus presented to an outside hospital with subjective fevers and progressive lower back pain radiating down her legs, inhibiting ambulation. Lumbar puncture studies were initially consistent with viral meningitis. Multiple blood and CSF cultures returned with MRSA. She received a 21-day course of vancomycin, rifampin, and claforan for MRSA meningitis. One week after discharge, the patient presented to our emergency department with a severe desquamating rash with underlying normal skin from the occiput to knees bilaterally, body aches, and dehydration. The rash began on her right upper extremity and spread globally, only sparing the mucous membranes, soles of the feet, and palms of the hands. Nikolsky9s sign was present. Laboratory upon admission revealed an elevated leukocyte count and BUN/Cr of 136/2.3. Skin biopsy revealed subcorneal splitting along the granular layer without dermal infiltration or organisms. MRSA was found in multiple blood cultures. She was treated with a 21-day course of vancomycin, maxipime, and rifampin; in addition, she was treated with aggressive wound care and intravenous hydration. During her hospital course, the patient9s skin rash resolved without scarring. Antibodies to TSST-1 and staphylococcal enterotoxin B were positive. Exfoliative toxins A and B were negative. MRSA was positive for Panton-Valentine leukocidin. Discussion SSSS occurs secondary to a systemic SA infection that produces bullous lesions that spare the mucous membranes. Nikolsky9s sign is typically positive. Exfoliative toxin A or B frequently causes the syndrome, but in the three reported cases involving MRSA, TSST-1 and circulating enterotoxin likely contribute to SSSS. Diagnostic criteria include SA-positive blood cultures, presence of SA toxins, skin biopsy, and clinical findings. Skin biopsy typically reveals subcorneal splitting along the granular layer without dermal infiltration. Treatment for SSSS includes anti-SA antibiotics, meticulous wound care, and aggressive fluid resuscitation. Despite aggressive therapy, the prognosis in adult cases is poor.

The management of tumor lysis syndrome

The manifestation of tumor lysis syndrome (TLS) occurs when the destruction of tumor cells releases breakdown products that overwhelm the excretory mechanisms of the body. A cardinal sign is hyperuricemia, leading to uric acid nephropathy. Other signs are hyperkalemia, hyperphosphatemia and secondary hypocalcemia. Conventional management of TLS consists of aggressive intravenous hydration, diuretic therapy, urinary alkalization, and inhibition of urate production by high-dose allopurinol. Urate oxidase has been used in the management of patients at risk for TLS and recently the recombinant urate oxidase rasburicase was developed. Several data indicate that rasburicase is effective and well tolerated in the prevention and treatment of chemotherapy-induced hyperuricemia. Treatment options of hyperkalemia include sodium polystyrene sulfonate, hypertonic glucose and insulin, loop diuretics, and bicarbonate. Treatment of hyperphosphatemia reduces dietary phosphate intake and includes phosphate binders such as aluminum hydroxide and aluminum carbonate. When recurrent hypocalcemia is present, a continuous intravenous infusion of calcium gluconate can be initiated. Hemodialysis should be considered for every patient with excessively elevated uric acid, phosphate and/or potassium and in those patients with acute renal failure to control urinary volume and manage uremia.

Lateral gluteal myonecrosis in a patient undergoing partial nephrectomy in the modified flank position

This is the first report of postoperative rhabdomyolysis occurring in a patient positioned in the “modified flank position,” with the kidney rest positioned under the top of the iliac crest. The patient was treated with aggressive intravenous fluid hydration and hyperbaric oxygen therapy with maintenance of normal renal function and near complete recovery of gluteal muscle function.