Acute pancreatitis is one of the main causes of intra-abdominal hypertension (IAH). IAH contributes to multiple physiologic alterations and leads to the development of abdominal compartment syndrome (ACS) that induces multiorgan failure. We report a case of ACS in a patient with severe acute pancreatitis. A 44-year-old man who was admitted in a drunk state was found to have severe acute pancreatitis. During management with fluid resuscitation in an intensive care unit, drowsy mentality, respiratory acidosis, shock requiring inotropes, and oliguria developed in the patient, with his abdomen tensely distended. With a presumptive diagnosis of ACS, abdominal decompression through percutaneous catheter drainage was performed immediately. The intraperitoneal pressure measured with a drainage catheter was 31 mm Hg. After abdominal decompression, the multiorgan failure was reversed. We present a case of ACS managed with percutaneous catheter decompression.
Abdomen ; Acidosis, Respiratory ; Adult ; Catheters* ; Decompression ; Diagnosis ; Drainage* ; Humans ; Intensive Care Units ; Intra-Abdominal Hypertension* ; Lower Body Negative Pressure ; Oliguria ; Pancreatitis* ; Resuscitation ; Shock ; Transcutaneous Electric Nerve Stimulation

An investigation of extrapulmonary oxygenation was made in dogs, rabbits and, finally, in a case of Tetralogy of Fallot using an intestinal perfusion of hydrogen peroxide (H2O2). For a single administration, 0.4 per cent H2O2 can be given safely by enema, in doses of 10ml./Kg. of body weight, this would give maximum oxygenation in both the portal vein and inferior vena cava without the formation of gas emboli. Concentrations higher than this caused gas bubbles in the portal vein. For serial administrations, 0.2 per cent H2O2 can be given by enema exchanging the intestinal contents at 10 to 15 minutes intervals. When given concomitantly with human whole blood, 1.0ml./Kg. of body weight, there is a prolonged higher oxygenation in the portal vein, inferior vena cava and femoral artery. This concentation of H2O2 would not cause gas emboli in the portal vein. Although extrapulmonary oxygenation is possible by giving oxygen by enema, this method would cause too much abdominal distension. In experiments of death by suffocation, the group given H2O2 had doubled the duration of E.K.G. activity when compared with controls. One patient with Tetralogy of Fallot, confirmed by clinical findings, X-ray studies, E.K.G. and cardiac catheterization, who was not suitable for cardiac surgery because of low mentality, was selected for this study. 0.2 per cent H2O2, 10ml. per Kg. of body weight by enema, exchanging intestinal contents at 30 minutes intervals, resulted in a marked elevation of the pO2 in the venous blood and in the inferior vena cava. There was a disappearance of finger tip and toe tip cyanosis and flushing of the soles and palms was noted during the procedure.
Acidosis, Respiratory/diagnosis ; Animals ; Asphyxia/therapy ; Carbon Dioxide/blood ; Child ; Dogs ; Enema ; Female ; Hematocrit ; Human ; Hydrogen Peroxide/administration & dosage/*therapeutic use ; Male ; Oxygen/blood ; Tetralogy of Fallot/*therapy

OBJECTIVE: The biochemical data of 10 patients admitted with diabetic ketoacidosis(DKA) during the last 2 years were analyzed for the disturbances of serum potassium(K) and acid-base balance with a special interest to look for the underlying causes of potassium(K) disorder, retrospectively. METHODS: Arterial blood gas analysis was done and electrolytes, serum glucose, serum osmolality, BUN, creatinine were checked on admission and recovery in 10 patients with diabetic ketoacidosis. RESULTS: The mean(+/-SE) serum K at diagnosis and on recovery was 4.9+/-0.9mEq/L(range, 3.2-6.5 mEq/L) and 3.8+/-0.2mEq/L(range, 3.0-4.3mEq/L), respectively. Hyperkalemia(>5.0mEq/L) in 30%(3/10) and hypokalemia(<3.5mEq/L) in 10%(1/10) was noted on admission, whereas, on recovery, hyperkalemia in none and hypokalemia in 40%(4/10). Initial K levels showed a negative correlation with pH(gamma= -0.62, P=0.05) but no significant correlation was found between the initial K levels with anion gap (AG), with serum glucose value and with blood osmolality. Only 40%(4/10) had a simple metabolic acidosis while 60%(6/10) had a mixed acid-base disorder DKA with respiratory alkalosis, mostly(5/6). The ratio of delta AG over delta HCO3 was not significantly different between patients with a simple metabolic acidosis(0.95) and with a mixed acid-base disorder(0.92). CONCLUSION: The degree of acidosis must be one of the predominant factors in the pathogenesis of the initial hyperkalemia rather than hyperglycemia resulting from insulinopenia itself. Also, we observed that patients with DKA commonly develop mixed acid- base disorders, and delta AG/delta HCO3 ratio would not be an useful tool to look for a mixed acid-base disorder.
Acid-Base Equilibrium* ; Acidosis ; Alkalosis, Respiratory ; Blood Gas Analysis ; Blood Glucose ; Creatinine ; Diabetic Ketoacidosis ; Diagnosis ; Electrolytes ; Humans ; Hyperglycemia ; Hyperkalemia ; Hypokalemia ; Osmolar Concentration ; Potassium* ; Retrospective Studies

The porphyrias are a group of disorders caused by deficiency in the enzymes of the heme biosynthetic pathway. Patients with porphyria may develop neurovisceral attacks which include severe abdominal pain, neuropsychiatric manifestations and potentially fatal respiratory paralysis. However, these patients may also have abdominal pain not due to porphyria itself, and in such case, careful evaluation is important. We report a case of acute pancreatitis with masquerading acute attack of porphyria, which made us difficult to make a correct diagnosis. A 29-year-old female, previously diagnosed to have hepatic porphyria, presented with acute abdominal pain, back pain and leg pain for 3 days. Serum amylase was normal and 24-hour urine -ALA and PBG showed increased levels. After intravenous infusion of glucose, symptoms were improved. From the 10th day of admission, she complained severe abdominal pain, and was found to have severe metabolic acidosis, shock, and signs of peritonitis on the 12th day of admission. Emergency exploration revealed edematous pancreas. Amylase and lipase levels in serum and ascites were found to be markedly elevated. After conservative management, her general condition gradually improved and serum amylase and lipase levels were normalized.
Abdomen, Acute ; Abdominal Pain ; Acidosis ; Adult ; Amylases ; Ascites ; Back Pain ; Biosynthetic Pathways ; Diagnosis ; Emergencies ; Female ; Glucose ; Heme ; Humans ; Infusions, Intravenous ; Leg ; Lipase ; Pancreas ; Pancreatitis* ; Peritonitis ; Porphyrias* ; Porphyrias, Hepatic ; Respiratory Paralysis ; Shock

Aspiration of meconium produces a syndrome (Meconium Aspiration Syndrome MAS) characterized by hypoxia, hypercapnia, and acidosis. Perinatal hypoxia, acute airway obstruction, pulmonary inflammation, pulmonary vasoconstriction, pulmonary hypertension, and surfactant inactivation all play a role in the pathogenesis of MAS. Most aspiration of meconium probably occurs before birth. Following aspiration, meconium may migrate to the peripheral airway, usually take about 2 hours as demonstrated in animal experiment, leading to airway obstruction and subsequent lung inflammation and pulmonary hypertension. The presence of meconium in the endotracheal aspirate automatically establishes the diagnosis of MAS. Clinical diagnosis can be made in any infant born with meconium staining of amniotic fluid who develops respiratory distress at or shortly after birth and has positive radiographic findings. Prevention of intrauterine hypoxia, early cleaning (suctioning) of the airway, and prevention and treatment of pulmonary hypertension are essential in the management of MAS. Recent studies suggest that avoidance of post-term delivery may reduce the risk of intrauterine hypoxia and the incidence of MAS. Routine intrapartum naso-and oropharyngeal suction does not appear to affect the incidence and outcome of MAS. Endotracheal suction at birth is considered a controversial procedure and only reserved for infants who have severe retraction at birth suggesting an upper airway obstruction. High frequency oscillatory ventilation with nitric oxide or surfactant may improve mortality. Mortality of MAS has improved; the causes of death are related primarily to hypoxic respiratory failure associated with irreversible pulmonary hypertension. Morbidity is affected mostly by perinatal hypoxia.
Acidosis ; Airway Obstruction ; Amniotic Fluid ; Animal Experimentation ; Anoxia ; Cause of Death ; Diagnosis ; Female ; Humans ; Hypercapnia ; Hypertension, Pulmonary ; Incidence ; Infant ; Infant, Newborn ; Meconium Aspiration Syndrome* ; Meconium* ; Mortality ; Nitric Oxide ; Parturition ; Pneumonia ; Respiratory Insufficiency ; Resuscitation* ; Suction ; Vasoconstriction ; Ventilation

To investigate whether hypercapnic acidosis, induced by adding CO2 to inspired gas, would be protective effect against ventilator-induced lung injury (VILI), we ventilated 55 normal white rabbits for 6 hr or until PaO2/FIO2 <200 mmHg. Control group (n=15) was ventilated with peak inspiratory pressure (PIP) of 15 cm H2O, positive end-expiratory pressure (PEEP) of 3 cm H2O, an inspiration-to-expiration ratio of 1:2, and an inspired oxygen fraction (FIO2) of 0.40. High pressure hypercapnic group (HPHC; n=20) was ventilated with PIP of 30 cm H2O, PEEP of 0 cm H2O, and FIO2 of 0.40. Carbon dioxide was introduced into the inspiratory limb of the ventilator circuit, as necessary to maintain hypercapnia (PaCO2, 65 to 75 mmHg). High pressure normocapnic group (HPNC; n=20) was ventilated with same setting of HPHC, except normocapnia (PaCO2, 35 to 45 mmHg). Bronchoalveolar lavage fluid (BALF) lactate dehydrogenase, aspartate aminotransferase, interleukin-8 were significantly higher in high pressure ventilator group than control group (p<0.05). Wet weight to dry weight (WW/DW) and histologic scores were significantly higher in high pressure ventilator group than control group (p<0.05). However, there were no significant differences in oxygenation, BALF inflammatory markers, WW/DW and histologic scores between HPHC and HPNC groups. These findings suggest that hypercapnic acidosis at least induced by CO2 insufflation would not be protective effect against VILI in this model.
Acidosis, Respiratory/*chemically induced/complications/diagnosis/physiopathology ; Administration, Inhalation ; Animals ; Carbon Dioxide/*administration and dosage ; Hypercapnia/*chemically induced/complications/diagnosis/physiopathology ; Inhalation ; Pulmonary Gas Exchange ; Rabbits ; Research Support, Non-U.S. Gov't ; Respiration, Artificial/*adverse effects ; Respiratory Distress Syndrome, Adult/diagnosis/*etiology/physiopathology/*prevention and control ; Treatment Outcome