1/28. Hypokalaemic, hyperchloraemic metabolic acidosis requiring ventilation.A 16-year-old patient required intermittent positive pressure ventilation for hypokalaemic muscle weakness resulting from metabolic complications of combined colonic bladder augmentation and incomplete voiding via a prosthetic sphincter. Catheter re-establishment of urinary flow and electrolyte replacement produced dramatic metabolic and clinical improvement allowing the return of adequate spontaneous respiration.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
2/28. neuroleptic malignant syndrome due to promethazine.A 42-year-old man came to our emergency room hyperthermic (oral temperature, 42.4 degrees C), diaphoretic, and delirious. Other findings included labile blood pressure, sinus tachycardia (heart rate, 138/min), tachypnea (respiratory rate 34/min), muscle rigidity, and incontinence. Two days earlier, he had gone to a local clinic with complaints of abdominal pain, nausea, and vomiting. promethazine was prescribed, and this was the patient's only medication on admission. Laboratory studies showed leukocytosis, hypernatremia, metabolic acidosis, elevated creatinine phosphokinase level, elevated transaminase levels, azotemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and myoglobulinuria. The clinical and laboratory findings were characteristic of the neuroleptic malignant syndrome, with promethazine as the offending agent.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
3/28. Continuous monitoring of cerebrospinal fluid acid-base balance and oxygen metabolism in patients with severe head injury: pathophysiology and treatments for cerebral acidosis and ischemia.INTRODUCTION: Continuous monitoring of cerebral acid-base balance and oxygen metabolism has been introduced in neurointensive care settings. The hypothesis of this study utilizing multimodal neuromonitoring modalities is that hyperventilation and hypothermia improve cerebral acidosis through prevention of cerebral ischemia aggravation in patients with severe head injury. patients AND methods: Continuous monitoring of cerebrospinal fluid (CSF) pH, PCO2, HCO3-, base excess (BE), PO2, SO2, temperature, lactate and pyruvate (La and Py) measurements were conducted in 8 patients with severe head injury. Temperature-corrected CSF parameters were correlated with those in the jugular blood including oxygen saturation (SjO2), regional oxygen saturation (rSO2), intracranial pressure (ICP) and cerebral perfusion pressure (CPP), jugular blood temperature (Tjb), and endtidal PCO2 (PetCO2). Therapeutic significance of hyperventilation and hypothermia was evaluated. RESULTS: 1) CSF acidosis was observed in all cases (minimum pH 6.59-7.17) due to increased CSF PCO2 and/or decreased CSF HCO3- and tended to associate with abnormal ICP and/or CPP or ischemic episodes indicated by CSF PO2 and SO2, rSO2, and/or SjO2 during monitoring. 2) It was more obvious in CSF than in jugular blood that increased PCO2, La and Py, and/or decreased HCO3- resulted in decreased BE and pH. 3) Decreased CSF PO2 and SO2 only correlated with severe CSF acidosis. 4) hyperventilation: Decreased PetCO2 did not always closely correlate with CSF PCO2 decrease and CSFpH increase. 5) hypothermia: There were negative correlations of Tjb with CSF pH and SO2 in all cases, though correlation coefficients were not always high. CONCLUSIONS: CSF acidosis caused by increased CSF PCO2, La and Py, and/or decreased HCO3- tended to associate with abnormal ICP and CPP, and desaturation indicated by CSF SO2, rSO2, and/or SjO2. hypothermia rather than hyperventilation tends to improve cerebral acidosis and ischemia.- - - - - - - - - - ranking = 2keywords = pressure (Clic here for more details about this article) |
4/28. Intradialytic hypercapnic respiratory failure managed by noninvasive assisted ventilation.We report a hemodialysis patient with acute hypercapnic respiratory failure managed on noninvasive intermittent positive pressure ventilation and progressive metabolic acidosis. Dialysate bicarbonate concentration of 25 mEq/l was associated with exacerbation of metabolic acidosis, while higher dialysate bicarbonate concentration of 30 mEq/l induced a dangerous increase in PCO(2) level. Excessive bicarbonate buffering and CO(2) production induced by severe metabolic acidosis, malnourishment and tissue hypoxia, could explain inadequate correction of metabolic acidosis and worsening of hypercapnia in this patient. Our findings suggest the need for close monitoring of blood gases and cautious modulation of dialysate bicarbonate concentration in the presence of progressive metabolic acidosis in hypercapnic hemodialysis patients.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
5/28. Metabolic acidosis, rhabdomyolysis, and cardiovascular collapse after prolonged propofol infusion.The authors present the hospital course of a 13-year-old girl with a closed head injury who received a prolonged infusion of propofol for sedation and, subsequently, died as a result of severe metabolic acidosis, rhabdomyolysis, and cardiovascular collapse. The patient had been treated for 4 days at a referring hospital for a severe closed head injury sustained in a fall from a bicycle. During treatment for elevations of intracranial pressure, she received a continuous propofol infusion (100 microg/kg/min). The patient began to exhibit severe high anion gap/low lactate metabolic acidosis, and was transferred to the pediatric intensive care unit at the authors' institution. On arrival there, the patient's glasgow coma scale score was 3 and this remained unchanged during her brief stay. The severe metabolic acidosis was unresponsive to maximum therapy. Acute renal failure ensued as a result of rhabdomyolysis, and myocardial dysfunction with bizarre, wide QRS complexes developed without hyperkalemia. The patient died of myocardial collapse with severe metabolic acidosis and multisystem organ failure (involving renal, hepatic, and cardiac systems) approximately 15 hours after admission to the authors' institution. This patient represents another case of severe metabolic acidosis, rhabdomyolysis, and cardiovascular collapse observed after a prolonged propofol infusion in a pediatric patient. The authors suggest selection of other pharmacological agents for long-term sedation in pediatric patients.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
6/28. A technique of anaesthesia in haemorrhagic shock. Illustrative case histories and a discussion.The anaesthetic management of patients in haemorrhagic shock is described. The principles are those of initial resuscitation with electrolyte solutions and alleviation of metabolic acidosis, combined with early induction of anaesthesia to permit control of bleeding as soon as possible. The anaesthetic technique depends on pre-oxygenation, intravenous anaesthesia, muscular relaxation and ventilation with pure oxygen. Earlier cases were induced with thiopentone and maintained with intermittent suxamethonium, but intravenous ketamine was later employed for induction and intramuscular ketamine for maintenance; this use of ketamine is now the author's method of choice. The use of a central venous pressure line connected to a cannula in the internal jugular vein is recommended.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
7/28. Non-specific hyperamylasemia in shosin beri-beri.Several reports demonstrate non-specific hyperamylasemia in cardiac surgery or diabetic ketoacidosis. We report here for the first time non-specific hyperamylasemia in a cardiovascular beri-beri case who showed shock with severe metabolic acidosis. Her echocardiography revealed hyperkinetic wall motion of the small left ventricle. Despite intravascular volume expansion in parallel with dopamine administration, her blood pressure did not recover. Abdominal computed tomography (CT) did not reveal pancreatic swelling or any other signs of acute pancreatitis. Her history suggested a possibility of cardiovascular beri-beri due to chronic alcoholism. thiamine administration dramatically reversed her haemodynamic derangements, metabolic acidosis and even relieved her abdominal pain. Isozyme examinations for hyperamylasemia showed that most of the serum amylase consisted of salivary type. This case report expands our information on non-specific hyperamylasemia encountered in the emergency setting.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
8/28. Is there an upper limit of intracranial pressure in patients with severe head injury if cerebral perfusion pressure is maintained?Authors of recent studies have championed the importance of maintaining cerebral perfusion pressure (CPP) to prevent secondary brain injury following traumatic head injury. Data from these studies have provided little information regarding outcome following severe head injury in patients with an intracranial pressure (ICP) greater than 40 mm Hg, however, in July 1997 the authors instituted a protocol for the management of severe head injury in patients with a glasgow coma scale score lower than 9. The protocol was focused on resuscitation from acidosis, maintenance of a CPP greater than 60 mm Hg through whatever means necessary as well as elevation of the head of the bed, mannitol infusion, and ventriculostomy with cerebrospinal fluid drainage for control of ICP. Since the institution of this protocol, nine patients had a sustained ICP greater than 40 mm Hg for 2 or more hours, and five of these had an ICP greater than 75 mm Hg on insertion of the ICP monitor and later experienced herniation and expired within 24 hours. Because of the severe nature of the injuries demonstrated on computerized tomography scans and their physical examinations, these patients were not aggressively treated under this protocol. The authors vigorously attempted to maintain a CPP greater than 60 mm Hg with intensive fluid resuscitation and the administration of pressor agents in the four remaining patients who had developed an ICP higher than 40 mm Hg after placement of the ICP monitor. Two patients had an episodic ICP greater than 40 mm Hg for more than 36 hours, the third patient had an episodic ICP greater than of 50 mm Hg for more than 36 hours, and the fourth patient had an episodic ICP greater than 50 mm Hg for more than 48 hours. On discharge, all four patients were able to perform normal activities of daily living with minimal assistance and experience ongoing improvement. Data from this preliminary study indicate that intense, aggressive management of CPP can lead to good neurological outcomes despite extremely high ICP. Aggressive CPP therapy should be performed and maintained even though apparently lethal ICP levels may be present. Further study is needed to support these encouraging results.- - - - - - - - - - ranking = 10keywords = pressure (Clic here for more details about this article) |
9/28. The electrocardiographic toxidrome: the ECG presentation of hydrofluoric acid ingestion.The clinician can approach the poisoned patient using the toxidrome system of toxin identification; this approach makes use of findings noted on the physical examination, highlighting the importance of abnormalities in blood pressure, heart rate, respiratory effort, body temperature, mental status, pupillary size, skin color, diaphoresis, and gastrointestinal sounds. Such a method provides structure and guidance to the clinical evaluation, providing the clinician with rapid diagnostic information and suggesting urgent management issues. A case of hydrofluoric acid poisoning is used as an example of this diagnostic approach. The patient demonstrated systemic toxicity accompanied by oral irritation and electrocardiographic abnormality (QRS complex widening and QT interval prolongation). The constellation of these findings suggested the possibility of a caustic agent (history and examination) with potential effect on potassium and calcium metabolism (electrocardiographic abnormalities). Such a constellation strongly suggested hydrofluoric acid as the culprit toxin.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
10/28. Metabolic acidosis induced by acetazolamide.The carbonic anhydrase inhibitors that are used most frequently in ophthalmic practice are acetazolamide and methazolamide. They both are weak systemic diuretics and lower intraocular pressure ultimately by decreasing aqueous production. Unfortunately, they have a number of important side effects including the potentiation or exacerbation of metabolic acidosis. In some patients, this pH shift may be quite transient and temporary; whereas, in some patients with other maladies, the acidosis may be much more serious. The patient herein reported had chronic obstructive pulmonary disease and had had a nephrectomy. Close patient monitoring is advisable in these types of patients.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
| | Next -> |