Metabolic acidosis case study

It is critical to differentiate acute and chronic respiratory acidosis, as the acute form is often a medical emergency that requires intubation and mechanical ventilation, whereas the chronic form is typically a stable condition. The blood gases in Case Study 2 came from a patient with advanced emphysema who is a "C02 retainer" due to ineffective ventilation. Because this patient s disease is chronic, the elevated PaC02 developed very slowly and allowed for metabolic compensation. 

A retrospective study of 38 cases of sodium fluoroacetate poisoning (including 7 deaths) concluded that hypotension and early-onset metabolic acidosis and increased serum creatinine were most often associated with poor short-term survival. ... 

These pediatric patients also suffered from clear signs of hypoxemia and renal failure (Azizi and Amid, 1990). Unfortunately, serum creatinine and renal function tests (RFTs) were not found in the charts. Arterial blood gases (ABGs) may provide useful information, but they may show a varied picture. In one pediatric study of mustard casualties, most (43%) cases showed a simple metabolic acidosis. The other groups showed showed the following ... 

Death. Cases of death in humans acutely exposed to airborne formaldehyde were not located. Death after the ingestion of fonnaldehyde (or a formalin solution) in humans has been reported in connection with attempted suicides. Metabolic acidosis has been noted prior to death, along with respiratory, cardiac, and renal failure autopsy revealed corrosive damage to gastrointestinal mucosa (Burkhart et al. 1990 Eells et al. 1981 Koppel et al. 1990). Increased rates of cancer-related mortality associated with occupational exposure to formaldehyde (predominately by inhalation) have been found in some epidemiological studies, but not in others (see Section 2.2.1.8 and Section 2.5). Animal studies indicate that subchronic inhalation exposure to concentrations below 20 ppm are not lethal (Feron et al. 1988 Maronpot et al. 1986 Martin 1990 Rusch et al. 1983 Saillenfait et al. 1989 Woutersen et al. 1987), but lifetime inhalation exposure to formaldehyde has been associated with early mortalities associated with... 

Vermeersch and co-workers have reported the case of a 4-month-old girl who presented with agitation, hyperexcitation, fever, dehydration, polypnea and metabolic acidosis. H NMR spectroscopy of the lyophilized urine from the patient showed the presence of 2-hydroxybenzoic acid (salicylic acid), o-hydroxyhippuric acid and 2,5-dihydroxyhippuric acid, which indicated that she had been poisoned with salicylate (aspirin). It is notable that this study was completed at 80 MHz, a relatively low field strength. 

Potential adverse effects associated with hypertonic fluid administration for circulatory insufficiency include cellular crenation and damage caused by the dramatic fluid shifts, as well as peripheral vein destruction from their high osmolality. Also, in the case of hypertonic sodium chloride solutions, there are the possibilities of neurologic damage from hypernatremia and hyperchloremic metabolic acidosis from hyperchloremia. In the limited number of studies conducted in humans to date, such adverse effects have been uncommon and apparently of little clinical importance. ... 

Acidosis occurs when the pH of blood falls below about 7.35. In respiratory acidosis, impaired respiration increases the concentration of dissolved CO2 and lowers the blood s pH. The condition is common in victims of smoke inhalation and patients with asthma, pneumonia, and emphysema. The most efficient treatment consists of placing the patient in a ventilator. Metabolic acidosis is caused by the release of large amounts of lactic acid or other acidic by-products of metabolism (Case study 43), which react with bicarbonate ion to form carbonic acid, thus lowering the blood s pH. The condition is common in patients with diabetes and severe burns. 

Haematologic adverse effects are mostly secondary to kidney dysfunction with some notable exceptions. Hyperchloraemic metabolic acidosis was induced in a 17-year-old patient with beta-thalassaemia on 30 mg/ kg daily deferasirox which resolved after removal of deferasirox [30 ]. The same study reviewed eight other cases of hyperchloraemic metabolic acidosis. The authors suggested that acidosis was the result of renal tubular dysfunction. 

All the polyoles have proved to exhibit undesirable or dangerous side effects in animal studies and when used therapeutically in man this has led in some countries (such as Australia) to a proliibi-tion on the use of xylitol for intravenous nutrition. Large quantities of fructose and sorbitol lead to a metabolic acidosis, the severity of which cannot be foreseen, as well as hyperuricaemia, and reduction in hepatic stores of nucleotide-adenine and inorganic phosphates. Xylitol produces identical effects (with hyperuricaemia being particularly pronounced) as well as osmotic diuresis with loss of electrolytes and, in some cases, formation of crystalline deposits in the kidneys and brain. 

Studies of the role of metabolic transporters in the control and modulation of metabolic fluxes have provided somewhat ambiguous results in the case of respiration and gluconeogenesis. The role of the glutamate transporter in the acute control of ammonia formation seems clear at this time, and a proposed role of the malate/a-ketoglutarate carrier in chronic acidosis is an intriguing possibility. 

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