Respiratory acidosis clinical presentation

Neurologic symptoms Motor weakness has been reported rarely. Most of these cases occurred in the setting of lactic acidosis. The evolution of motor weakness may mimic the clinical presentation of Guillain-Barre syndrome (including respiratory failure). Symptoms may continue or worsen following discontinuation of therapy. Stavudine therapy has been associated with peripheral neuropathy, which can be severe and is dose-related. Peripheral neuropathy has occurred more frequently in patients with advanced HIV disease, a history of neuropathy, or concurrent neurotoxic drug therapy, including didanosine (see Adverse Reactions). 

II. Toxic dose. Inhalation or ingestion of as little as 1 mg of fluoroacetate is sufficient to cause serious toxicity. Death is likely after ingestion of mote than 5 mg/kg. Clinical presentation. After a delay of minutes to several hours (in one report coma was delayed 36 hours), manifestations of diffuse cellular poisoning become apparent nausea, vomiting, diarrhea, metabolic acidosis, renal failure, agitation, confusion, seizures, coma, respiratory arrest, pulmonary edema, and ventricular arrhythmias may occur. One case series reported a high incidence of hypocalcemia and hypokalemia. 

Benzyl alcohol is a preservative that may be present in multidose vials of bacteriostatic sodium chloride and bacteriostatic water for injection and pharmaceuticals available in multidose vials for parenteral use. An association between the presence of benzyl alcohol in solutions used for flushing intravascular catheters and to reconstitute medications and a gasping syndrome and deaths in neonates was first reported in the early 1980s.The neonates also displayed clinical findings such as an elevated anion gap, metabolic acidosis, CNS depression, seizures, respiratory failure, renal and hepatic failures, cardiovascular collapse, and death. Those at highest risk were premature infants who weighted less... 

Hyperosmolar hyperglycaemia (HH) is generally the fulminant result of poorly treated type 2 diabetes or delayed diagnosis of previously unknown type 2 diabetes. HH is less frequent than DKA, but mortality is higher and remains close to 15% in many centres [1,20]. As implied hyperosmolality is the primary clinical problem and there will be hyperglycaemia of >35 0 mmol/L and an effective seram osmolality of >320 mOsm/kg (Table 1). HH most often occurs in frail patients in combination with other potentially fatal conditions. Strict differentiation between DKA and HH can be difficult, because some degree of ketosis may be present in HH and because, for example, lactic acidosis, respiratory and renal failure may also be present. In practise this dilemma is mainly ornamental, since diagnostic and therapeutic efforts follow the same principles. 

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