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DISORDERS OF OESOPHAGEAL MOTILITY IN CHRONIC HAEMODIALYSIS PATIENTS
219 DISORDERS OF OESOPHAGEAL MOTILITY IN CHRONIC HAEMODIALYSIS PATIENTS
SIR,-In the past 13 months we have investigated symptoms of oesophageal disease in four of our fifty-six chronic haemodialysis patients and in a fifth patient referred to us. All five patients had oesophageal dysmotility, a previously unreported complication of chronic uraemia. Patients with symptoms suggestive of oesophageal dysmotility were investigated by barium swallow studies and then by manometry (four patients) and/or oesophagoscopy (three). For manometry we used a 120 cm motility probe (P-31-305; Konigsberg Instruments) with a probe diameter 0[5mm. The transducers were arranged to measure intratuminat pressure at three points 5 cm apart and at 120° to each other. The recording assembly was moved 0’ 5 cm at a time from the stomach through the gastro-oesophageal high pressure zone (LES) and then 1 cm at a time through the oesophagus. LES pressures were recorded with midrespiratory pressure with a mean gastric fundic pressure as the zero reference. Oesophageal contractions were timed and amplitudes of oesophageal contractions were measured. Normal LES pressure in our laboratory is 10-20 mm Hg, with total relaxation of LES pressure on swallowing. Normal peristaltic waves are uniphasic and progressive. An "abnormal" amplitude is not
easy to define but values two or more standard deviations from the mean. considered definitely abnormal.
were
Investigations are summarised in the table; and details of cases 1 and 5 are as follows: Case 1.-This woman with end-stage renal disease presented with a 1-year history of nausea, vomiting, subxiphoid pain, and dysphagia which had started 2 months after haemodialysis had been instituted. A change to continuous ambulatory peritoneal dialysis had not improved her gastrointestinal symptoms. Manometry revealed normal peristaltic contractions of normal amplitude and velocity of propagation in the upper third of the oesophagus. With deglutition, an occasional peristaltic contraction of the lower twothirds of the oesophagus was noted. However, most smooth muscle contractions were simultaneous and repetitive, with two or three peaks, and normal in amplitude and duration. Spontaneous contractions were noted. LES was raised. There was prompt and complete relaxation with deglutition. Treatment with oral nitrates before meals was followed by clinical improvement. Case 5.-This woman had been on chronic haemodialysis for 3 years and had a 3-month history of dysphagia. Barium studies revealed a severe narrowing of the oesophagogastric junction, with dilatation of the proximal oesophagus and no peristaltic activity (confirmed by manometry). The abnormal LES did not decrease to baseline with wet or dry swallows. Achalasia was diagnosed. Because of her severe hypertensive cardiomyopathy and the spontaneous improvement in her symptoms, no definitive treatment was
given.
Thus 7% of our dialysis outpatients have oesophageal motility disorders. Since we did investigations only on patients who volunteered oesophageal symptoms, oesophageal abnormalities may be even more common in these patients. These patients were not diabetic or alcoholic and they had no signs of intestinal pseudo-
obstruction. None of our chronic haemodialysis patients has had dialysis dementia and the dialysate water supply is treated by reverse osmosis and mixed bed deionisation, so aluminium intoxication is unlikely to have played a role. Axonal degeneration affecting the vagus nerve has been reported in achalasia and in diffuse oesophageal spasm;2-4 and Beck and DaCostahave suggested that diffuse oesophageal spasm results from denervation in the body of the oesophagus, the denervation progressing to the lower oesophageal sphincter, thus leading to achalasia. Uraemic neuropathy is not well understood, but axonal degeneration is generally thought to be the underlying lesion. 6, We suggest that, in the five patients described, chronic renal failure resulted in axonal denervation and uraemic neuropathy of the vagus nerve, manifesting as oesophageal spasm and achalasia. Patient 3 has sleep apnoea. Sleep apnoea has been reported as a complication of medullary infarction.8,9 Since the dorsal motor nucleus of the vagus nerve and the medullary respiratory centre are close to each other, perhaps an ischaemic insult to the medulla resulted in both achalasia and central sleep apnoea in this patient. We suspect that abnormal oesophageal motility contributes to the vomiting so frequently, and in some cases incorrectly, ascribed to dysequilibrium or to underdialysis in haemodialysis patients. Department of Medicine, Divisions of Gastroenterology and Nephrology, Thomas Jefferson University Hospital, Philadelphia, 19107 Pennsylvania, USA
GEORGE C. FRANCOS ANATOLE BESARAB RAYMOND E. JOSEPH
OESOPHAGEAL TRANSECTION FOR VARICEAL BLEEDING
SiR,-We agree with Dr Rose and Dr Smith (Jan 7, p 52) that conservative medical management alone for acute variceal bleeding is not acceptable, and are equally concerned about the prevention of early deaths from haemorrhage before injection sclerotherapy becomes effective. Our experience in 53 patients treated by oesophageal transection for haemorrhage uncontrolled by conserAluminum neurotoxicity: Experimental perspective. Bull Environ Contam Toxicol 1982; 29: 43-49. 2. Cassella RR, Ellis HF, Brown AL. Diffuse spasm of the lower part of the oesophagus: Fine structure of oesophageal smooth muscle and nerve. JAMA 1965; 191: 379-82. 3. Cassella RR, Ellis FH, Brown AL. Fine structure changes in achalasia of the oesophagus. Am J Pathol 1965: 46: 279-88. 4. Cassella RR, Brown AL, Sayre GP, Ellis FH. Achalasia of the esophagus: Pathologic and etiologic considerations. Ann Surg 1964; 160: 474-86. 5 Beck IT, DaCosta LR. Diffuse spasms and achalasia. J Clin Gastroenterol 1979; 1: 287-88. 6. Thomas PK, Hollinrake K, Lascalles RG, O’Sullivan DJ, Baillod RA, Moorhead JF, Mackenzie JC. The polyneuropathy of chronic renal failure. Brain 1971; 94:
1. Marquis JK.
761-80. 7.
8.
Dyck PJ, Johnson WJ, Lambert EH, O’Brien PC. Segmental demyelination secondary to axonal degeneration in uremic neuropathy. Mayo Clin Proc 1971; 46: 400-31. Devereaux MW, Keane JR, Davis RL. Automatic respiratory failure associated with infarction of the medulla. Arch Neurol 1973; 29: 47-52. BE, Margolis G. Acute failure of automatic respirations secondary to a unilateral brain stem infarct. Ann Neurol 1977; 1: 583-86.
9. Levin
CLINICAL DATA* AND SUMMARY OF INVESTIGATIONS
* Cases 1, 3, 4, and 5 had hypertensive glomerulosclerosts, case 2 had polycystic kidneys. DES=dtfFuse oesophageal spasm, V=vomiting, D=dysphagia, P=pyrosis, O=odynophagia, R=regurg1tatlon
SIR,-In the past 13 months we have investigated symptoms of oesophageal disease in four of our fifty-six chronic haemodialysis patients and in a fifth patient referred to us. All five patients had oesophageal dysmotility, a previously unreported complication of chronic uraemia. Patients with symptoms suggestive of oesophageal dysmotility were investigated by barium swallow studies and then by manometry (four patients) and/or oesophagoscopy (three). For manometry we used a 120 cm motility probe (P-31-305; Konigsberg Instruments) with a probe diameter 0[5mm. The transducers were arranged to measure intratuminat pressure at three points 5 cm apart and at 120° to each other. The recording assembly was moved 0’ 5 cm at a time from the stomach through the gastro-oesophageal high pressure zone (LES) and then 1 cm at a time through the oesophagus. LES pressures were recorded with midrespiratory pressure with a mean gastric fundic pressure as the zero reference. Oesophageal contractions were timed and amplitudes of oesophageal contractions were measured. Normal LES pressure in our laboratory is 10-20 mm Hg, with total relaxation of LES pressure on swallowing. Normal peristaltic waves are uniphasic and progressive. An "abnormal" amplitude is not
easy to define but values two or more standard deviations from the mean. considered definitely abnormal.
were
Investigations are summarised in the table; and details of cases 1 and 5 are as follows: Case 1.-This woman with end-stage renal disease presented with a 1-year history of nausea, vomiting, subxiphoid pain, and dysphagia which had started 2 months after haemodialysis had been instituted. A change to continuous ambulatory peritoneal dialysis had not improved her gastrointestinal symptoms. Manometry revealed normal peristaltic contractions of normal amplitude and velocity of propagation in the upper third of the oesophagus. With deglutition, an occasional peristaltic contraction of the lower twothirds of the oesophagus was noted. However, most smooth muscle contractions were simultaneous and repetitive, with two or three peaks, and normal in amplitude and duration. Spontaneous contractions were noted. LES was raised. There was prompt and complete relaxation with deglutition. Treatment with oral nitrates before meals was followed by clinical improvement. Case 5.-This woman had been on chronic haemodialysis for 3 years and had a 3-month history of dysphagia. Barium studies revealed a severe narrowing of the oesophagogastric junction, with dilatation of the proximal oesophagus and no peristaltic activity (confirmed by manometry). The abnormal LES did not decrease to baseline with wet or dry swallows. Achalasia was diagnosed. Because of her severe hypertensive cardiomyopathy and the spontaneous improvement in her symptoms, no definitive treatment was
given.
Thus 7% of our dialysis outpatients have oesophageal motility disorders. Since we did investigations only on patients who volunteered oesophageal symptoms, oesophageal abnormalities may be even more common in these patients. These patients were not diabetic or alcoholic and they had no signs of intestinal pseudo-
obstruction. None of our chronic haemodialysis patients has had dialysis dementia and the dialysate water supply is treated by reverse osmosis and mixed bed deionisation, so aluminium intoxication is unlikely to have played a role. Axonal degeneration affecting the vagus nerve has been reported in achalasia and in diffuse oesophageal spasm;2-4 and Beck and DaCostahave suggested that diffuse oesophageal spasm results from denervation in the body of the oesophagus, the denervation progressing to the lower oesophageal sphincter, thus leading to achalasia. Uraemic neuropathy is not well understood, but axonal degeneration is generally thought to be the underlying lesion. 6, We suggest that, in the five patients described, chronic renal failure resulted in axonal denervation and uraemic neuropathy of the vagus nerve, manifesting as oesophageal spasm and achalasia. Patient 3 has sleep apnoea. Sleep apnoea has been reported as a complication of medullary infarction.8,9 Since the dorsal motor nucleus of the vagus nerve and the medullary respiratory centre are close to each other, perhaps an ischaemic insult to the medulla resulted in both achalasia and central sleep apnoea in this patient. We suspect that abnormal oesophageal motility contributes to the vomiting so frequently, and in some cases incorrectly, ascribed to dysequilibrium or to underdialysis in haemodialysis patients. Department of Medicine, Divisions of Gastroenterology and Nephrology, Thomas Jefferson University Hospital, Philadelphia, 19107 Pennsylvania, USA
GEORGE C. FRANCOS ANATOLE BESARAB RAYMOND E. JOSEPH
OESOPHAGEAL TRANSECTION FOR VARICEAL BLEEDING
SiR,-We agree with Dr Rose and Dr Smith (Jan 7, p 52) that conservative medical management alone for acute variceal bleeding is not acceptable, and are equally concerned about the prevention of early deaths from haemorrhage before injection sclerotherapy becomes effective. Our experience in 53 patients treated by oesophageal transection for haemorrhage uncontrolled by conserAluminum neurotoxicity: Experimental perspective. Bull Environ Contam Toxicol 1982; 29: 43-49. 2. Cassella RR, Ellis HF, Brown AL. Diffuse spasm of the lower part of the oesophagus: Fine structure of oesophageal smooth muscle and nerve. JAMA 1965; 191: 379-82. 3. Cassella RR, Ellis FH, Brown AL. Fine structure changes in achalasia of the oesophagus. Am J Pathol 1965: 46: 279-88. 4. Cassella RR, Brown AL, Sayre GP, Ellis FH. Achalasia of the esophagus: Pathologic and etiologic considerations. Ann Surg 1964; 160: 474-86. 5 Beck IT, DaCosta LR. Diffuse spasms and achalasia. J Clin Gastroenterol 1979; 1: 287-88. 6. Thomas PK, Hollinrake K, Lascalles RG, O’Sullivan DJ, Baillod RA, Moorhead JF, Mackenzie JC. The polyneuropathy of chronic renal failure. Brain 1971; 94:
1. Marquis JK.
761-80. 7.
8.
Dyck PJ, Johnson WJ, Lambert EH, O’Brien PC. Segmental demyelination secondary to axonal degeneration in uremic neuropathy. Mayo Clin Proc 1971; 46: 400-31. Devereaux MW, Keane JR, Davis RL. Automatic respiratory failure associated with infarction of the medulla. Arch Neurol 1973; 29: 47-52. BE, Margolis G. Acute failure of automatic respirations secondary to a unilateral brain stem infarct. Ann Neurol 1977; 1: 583-86.
9. Levin
CLINICAL DATA* AND SUMMARY OF INVESTIGATIONS
* Cases 1, 3, 4, and 5 had hypertensive glomerulosclerosts, case 2 had polycystic kidneys. DES=dtfFuse oesophageal spasm, V=vomiting, D=dysphagia, P=pyrosis, O=odynophagia, R=regurg1tatlon