Respiratory decompensation

The treatment of respiratory acidosis is dependent on the chronicity of the patient s condition. Respiratory decompensation in patients with chronic elevations in PaC02 are frequently seen in those with acute infections and those recently started on narcotic analgesics or oxygen therapy. Aggressive treatment of these conditions can offer considerable benefit and should be initiated. Furthermore, tranquilizers and sedatives should be avoided and supplemental oxygen, if used, should be minimized. 

Phase II begins 60 minutes into the seizure, and the patient begins to decompensate. The patient may become hypotensive, and cerebral blood flow may be compromised. Glucose may be normal or decreased, and hyperthermia, respiratory deterioration, hypoxia, and ventilatory failure may develop. 

Underlying respiratory disease Zanamivir has not been shown to be effective and may carry risk in patients with severe or decompensated COPD or asthma, and serious adverse events have been reported in such patients. Therefore, zanamivir is not generally recommended for treatment of patients with underlying airways disease such as asthma or COPD. 

The most common adverse effects of lamivudine seen at doses used to treat HBV are mild they include headache, malaise, fatigue, fever, insomnia, diarrhea, and upper respiratory infections. Elevated alanine aminotransferase (ALT), serum lipase, and creatine kinase may also occur. The safety and efficacy of lamivudine in patients with decompensated liver disease have not been established. Dosage adjustment is required in individuals with renal impairment. Coadministration of trimethoprim-sulfamethoxazole decreases the renal clearance of lamivudine. 

A 43-year-old woman was admitted to hospital in December feeling unwell with a two-week history of urinary symptoms. She had decompensated cirrhosis of her liver on ultrasound and was taking pentoxifylline (oxpentifylline, Trental), co-amoxiclav, omeprazole and thiamine. She was jaundiced and confused with respiratory failure limiting speech to partial sentences. There was a marked deterioration in liver function overnight and she went into acute renal failure. 

A 42-year-old woman who presented with a change in mental status and rapidly decompensated into respiratory failure and required ventilatory assistance for 2 months had not taken an overdose—her lithium concentration had increased slowly (567). 

Patients with cirrhosis often suffer from bacterial infections, (s. p. 731) In most cases, the respiratory tract and urogenital system are affected. Interleukin 6 may often increase in decompensated cirrhosis. Directed bacteriological diagnosis is required immediately depending on the case, administration of antibiotics is recommended even before any evidence of bacteria has been obtained. (31)... 

In order to secure the patient s airway, intubation is necessary in cases of respiratory distress from Jaryngospasm, bronchospasm, or severe bronchorrhea. Regular monitoring of neck muscle weakness, respiratory rate, arterial blood gas, and menial status is required to assess progression or decompensation. The tidal volume initiated by the patient can be used as a measure of disease severity in those who are intubated. 

Wernicke s encephalopathy is associated with a mortality rate of 10-20%, predominantly as a result of sepsis, respiratory infection and decompensated liver disease Korsakoff s psychosis is associated with a mortality rate of approximately 17% (Harrison et al, 2006 Ogershok et al, 2002 Meikin-Zaborsky et al, 2001). 

Fatty acid )5-oxidation defects often have an episodic character. In between the attacks of metabolic decompensation, plasma and urine parameters tend to virtually normal. On the other hand, several conditions have been recognized to yield metabolite profiles similar to those of fatty acid oxidation defects. Amongst these are feeding with medium-chain triglyceride containing feedstuffs, gastro-intestinal problems such as coeliac disease, and dysfunction of the respiratory chain. 

A previous study (14) has suggested that nocturnal MTV could be used as an interim measure in subjects with severe OSA and hypercapnia until ventilatory decompensation is reversed (possibly by alterations in ventilatory drive and ventilatory responses to hypercapnia and hypoxia) and CPAP therapy can then be used long term. Others (30) have shown that a proportion of patients may be switched over to CPAP once respiratory failure has been controlled. CPAP therapy from the start, rather than bi-level ventilation followed by CPAP, may be just as effective (particularly improving sleep architecture and arousals) and potentially more cost-effective in patients with OHS, even if blood gases are not corrected immediately. 

Shivaram U, Cash ME, Beal A. Nasal continuous positive airway pressure in decompensated hypercapnic respiratory failure as a complication of sleep apnea. Chest 1993 104 770-774. Sturani C, Galavotti Y, Scarduelli C, et al. Acute respiratory failure due to severe obstructive sleep apnea syndrome, managed with nasal positive pressure ventilation. Monaldi Arch Chest Dis 1994 49 558-560. 

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