Mechanism of sleep-induced periodic breathing in convalescing stroke patients and healthy elderly subjects.

Cerebral vascular ischemic strokes are known to precipitate Cheyne-Stokes periodic breathing. Interestingly, Cheyne-Stokes-like breathing during sleep may be associated with obstructive sleep apnea (OSA) in some individuals. Therefore, it was reasoned that stroke patients with periodic breathing in sleep would be susceptible to OSA. Because oscillations in upper airway resistance can occur as a component of sleep-induced periodic breathing, we hypothesized that stroke patients with sleep-induced periodic breathing would have oscillations in upper airway resistance. These oscillations in resistance would be expected to contribute to OSA. We studied stroke patients with sleep-induced periodic breathing and control subjects to evaluate the relationship between upper airway resistance and ventilation in periodic breathing in sleep. Ventilation and upper airway resistance were measured in presleep wakefulness and in stage 2 NREM sleep. Mean tidal volume, minute ventilation, respiratory cycle timing variables, and upper airway resistance were not different between stroke and control subjects, either awake or asleep. Upper airway resistance increased and ventilation volume decreased from wakefulness to sleep in both groups. In an equivalent number of subjects from each group, reciprocal patterned oscillations in tidal volume and upper airway resistance were present at a 5 to 12.5 breath frequency during sleep. As upper airway resistance increased, tidal volume decreased. Stroke patients had wider fluctuations in upper airway resistance than control subjects, likely contributing to the higher number of sleep-disordered breathing events observed in the stroke patients.

Deep vein thrombosis in stroke patients: An overview.

Deep vein thrombosis (DVT) is prevalent both in the acute and the later phases of stroke. From previous studies using (125)I fibrinogen uptake, its peak incidence appears to occur during the first 10 days of stroke. Using venography and impedance plethymography, its prevalence is still high (between 30% and 40%) 1 1/2 to 6 months after stroke. The incidence of pulmonary embolism appear to diminish after the acute phase of stroke. Venous stasis is a widely accepted factor in the cause of DVT. More recently, venous injury as endothelial damage from excessive venodilation has been postulated. Increased venous size in hemiplegic limb has been reported. Further studies as to the role of decreased venous velocity and increased venous size and the effect of various modalities influencing these effects are needed. Routine screening of stroke patients appears indicated, but what protocol should be followed has yet to be determined. Selective screening by stratifying patients as to their clinical risk may be appropriate if found safe and cost-effective. Prophylactic treatment should be initiated in patients who are at increased risk of DVT. The prophylaxis of venous thrombosis in stroke patients remains uncertain. The use of low-molecular heparin may be a promising option if it is proven safe, efficacious, and causes less bleeding. Other prophylactic methods remain to be investigated.

The elderly amputee with severe chronic obstructive pulmonary disease. Case reports.

The case reports describe three elderly amputees with coexisting severe COPD. All three successfully mastered their prostheses and were discharged home able to walk functional distances. This demonstrates that these patients deserve a trial period of rehabilitation in a situation where close medical supervision and optimal medical management are available. Two of our cases died within 5 years, indicating the fragility and poor long-term prognosis of these patients; the third was lost to follow-up.

Occult proximal deep vein thrombosis: its prevalence among patients admitted to a rehabilitation hospital.

This study was designed first to determine the prevalence of occult proximal deep vein thrombosis (DVT) in stroke patients admitted to rehabilitation hospital using the technique of impedance plethysmography (IPG), and second, to identify clinical findings which may be indicators of an increased risk for the development of proximal DVT. Impedance plethysmography was performed on 105 consecutive stroke patients within one week of admission to our hospital. It was found that 34 out of 100 patients with adequate studies had abnormal IPG, two out of the 34 had known DVT, leaving 32 out of 98 with undiagnosed DVT (19 on the paretic side alone, nine bilateral, and four on the nonparetic side). Using logistic regression analysis, it was determined that profound weakness, male gender, interval between the stroke and IPG, edema, and leg hyperpigmentation were independently associated with positive IPG. Since IPG has a high positive predictive value for proximal DVT, one must assume that most of our patients with positive IPG have proximal DVT. Routine screening of stroke patients for DVT seems indicated and probably should include noninvasive venous studies such as serial IPG. The most efficient screening protocol needs to be determined.