Phrenic neuropathy in chronic renal failure.

Zifko, Udo; Auinger, Martin; Albrecht, Günter; Kästenbauer, T; Lahrmann, Heinz; Grisold, Wolfgang; Wanke, T.

doi:10.1136/thx.50.7.793

Cited by 25 publications

(10 citation statements)

References 8 publications

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“…Since our patient was managed by noninvasive ventilation, such a decrease in respiratory drive might have contributed to the exacerbation of hypercapnia. In addition, there is evidence for decreased ventilatory reserve in dialysis patients, including decreased ventilatory response to hypercapnia in HD patients with autonomic neuropathy [11] and phrenic nerve neuropathy in almost 50% of HD patients [12]. Though intradialytic oxygen administration does not usually affect ventilation and can prevent hypoxia [13,14], since avoiding high PO 2 levels might contribute to minute ventilation in the presence of PCO 2 149 mm Hg [15], the patient was initially maintained without supplemental oxygen.…”

Section: Discussionmentioning

confidence: 99%

Intradialytic Hypercapnic Respiratory Failure Managed by Noninvasive Assisted Ventilation

Tovbin

Heimer

Mashal³

et al. 2001

Am J Nephrol

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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 PCO₂ level. Excessive bicarbonate buffering and CO₂ 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.

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Section: Discussionmentioning

confidence: 99%

Intradialytic Hypercapnic Respiratory Failure Managed by Noninvasive Assisted Ventilation

Tovbin

Heimer

Mashal³

et al. 2001

Am J Nephrol

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“…Bilateral diaphragmatic paralysis can occur from motor neuron disease, myopathy, acid maltase deficiency, lupus (shrinking lung syndrome), end-stage renal disease, hypo or hyperthyroidism and malnutrition [ 5 ]. Diabetes by itself can cause phrenic nerve neuropathy and this has been reported in the literature [ 6 ].…”

Section: Discussionmentioning

confidence: 99%

Osteoarthrosis causing altered mental status: a case report

Reddy

2014

J Med Case Reports

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IntroductionCervical spondylosis as a cause of diaphragmatic weakness is an uncommon entity and has been reported primarily in the setting of cervical spinal cord compression. Cervical spondylosis most often causes respiratory failure from cervical myelopathy and damage to the ventral horn cells at spinal cord segments C3 to C5 from where the phrenic nerve arises. The manifestations are variable but there may be evidence of upper motor neuron signs and neurological deficits in the lower extremities along with Lhermitte’s sign. Here we report a rare case of cervical spondylosis causing phrenic nerve root compression from foraminal narrowing at C3, C4 and C5, leading to lower motor neuron paralysis of the phrenic nerve and respiratory failure, in the absence of spinal cord involvement.Case presentationAn 87-year-old Caucasian man presented with recurrent episodes of hypercapnic respiratory failure and altered mental status requiring intubation. He was noted to have neurological deficits in his upper extremities with C5 radiculopathy deficits. An arterial blood gas showed a normal alveolar-arterial oxygen gradient with chronic respiratory acidosis, and pulmonary function testing showed restrictive lung mechanics with weakened neuromuscular apparatus and low maximum inspiratory and expiratory pressures. An extensive workup including electromyogram and magnetic resonance imaging showed evidence of phrenic neuropathy secondary to C3 to C5 neural foramina compression, from cervical spondylosis. He was treated conservatively with night-time bilevel positive airway pressure which rested his respiratory musculature with significant improvement.ConclusionsCervical spondylosis leading to phrenic nerve root compression is a rare and underreported cause of chronic respiratory acidosis and must be considered in the differential diagnosis of chronic hypoventilation, particularly in the elderly. This case illustrates how a simple arterial blood gas and calculation of the alveolar-arterial oxygen gradient can help in the workup of chronic respiratory acidosis by identifying causes of hypoventilation, which are associated with a normal diffusing lung capacity and thereby a normal alveolar-arterial oxygen gradient.

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“…Hence, conduction velocitiesmay be moderately reduced and distal latenciesprolonged. Phrenic nerve latencies are also prolonged inuremia (5). Compound muscle action potentialamplitudes and sensory action potential amplitudes are theearliest to be involved, along with prolongation of H orF wave latencies.…”

Section: Uremic Polyneuropathymentioning

confidence: 99%

Neurologic Complications of End‐Stage Renal Disease: Peripheral Nervous System Complications in Hemodialysis Patients

Young

1997

Seminars in Dialysis

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Phrenic neuropathy in chronic renal failure.

Abstract: Background -Peripheral neuropathy and alterations in diaphragmatic muscle function are frequently caused by uraemia. Phrenic nerve function in patients with end stage renal failure, however, has not

Cited by 25 publications

References 8 publications

Intradialytic Hypercapnic Respiratory Failure Managed by Noninvasive Assisted Ventilation

Intradialytic Hypercapnic Respiratory Failure Managed by Noninvasive Assisted Ventilation

Osteoarthrosis causing altered mental status: a case report

Neurologic Complications of End‐Stage Renal Disease: Peripheral Nervous System Complications in Hemodialysis Patients

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