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LACTICACIDOSIS AND THIAMINE DEFICIENCY
1282
Although
this patient had mild mitral regurgitation there seems think this was other than a "sudden death" from asthma. Her variable airways obstruction had always responded to treatment previously when she sought medical help. It is felt this patient had inappropriate expectations of relief from repeated nebulised salbutamol when in fact she had become bronchodilator resistant. Nebulisers merely provide an alternative method of administering aerosol bronchodilator in much larger doses than the standardised pressurised aerosols. If airways do not respond additional treatment and admission to hospital are urgently needed. Her death is all the more disappointing since she had received and seemed to understand full instructions from her general practitioner about the dangers of nebuliser therapy. She had been given contingency instructions but for reasons that we shall never know she failed to comply with them. Patients with acute severe asthma who delay calling for medical assistance after a standard dose of nebulised bronchodilator has not given the expected relief are at risk of death from their disease. no reason to
The only certain way to exclude thiamine deficiency as a cause of a patient’s acute illness is not by the dietary history or even by estimation of the red blood cell transketolase activity but by the lack of response to an intravenous injection of thiamine. Was this test done in Huckabee’s cases? Another case of spontaneous lacticacidosis may have been a case of APB8 while there is doubt about the aetiology of a second case because of the apparent 9 response to intravenous methylene-blue.9 The Hospital, Alice Springs
New Territory 5750, Australia
I. S. PETHERAM
Newport
D.
F. JONES
LACTICACIDOSIS AND THIAMINE DEFICIENCY
Langen CD, Lichtenstein A. A clinical text-book of tropical medicine. Batavia Amsterdam: G Kolff, 1936: 393-421 Platt BS. Thiamine deficiency in human beriberi and in Wernicke’s encephalopathy In. Wolstenholme GEW, O’Connor M eds. Thiamine deficiency: Biochemical lesions and their clinical significance London J & A Churchill, 1967; 135-45 Platt BS Biochemical changes, especially of pyruvic acid, in relation to some clinical features of beriberi Trans Roy Soc Trop Med Hyg 1938; 31: 493-501 Huckabee WE Abnormal resting blood lactate I: the significance of hyperlactatemia in hospitalized patients. Am J Med 1961; 30: 833-39 Huckabee WE. Abnormal resting blood lactate II Lactic acidosis. Am J Med 1961; 30: 840-48. King JF, Easton R, Dunn M Acute pernicious beriberi heart disease. Chest 1972, 61:
1. De 2
3. 4
5.
Newport Chest Clinic, Newport, Gwent, NPT 4GA
CHARLES H. CAMPBELL
6.
512-14 7 Fond B, Richard C, Comoy E, Tillement JP, Auzepy P Two cases of shoshin beri beri with hemodynamic and plasma catecholamine data Intensive Care Med 1980, 6:
193-98.
regard the patients with acute pernicious beriberi (APB) as cases of hepatorenal syndrome, as Dr Anderson (Sept 15, p 644) suggests. Only one patient (case 18) was in liver failure and there are valid explanations for the renal failure of APB other than severe liver disease. The compensatory respiratory alkalosis to which Dr Hoorntje and Dr Hillen (Oct 6, p 807) draw our attention highlights the extreme hyperpnoea and the dyspnoea which are the dominant sign and the commonest symptom of APB. Even though lactic acid may accumulate in ordinary cases of beriberi heart disease and a syndrome of severe lacticacidosis, identical to APB, may complicate established beriberi, possibly the term APB should be restricted to the acute development of severe lacticacidosis in a person with no preceding symptoms of beriberi. (My cases 12, 17, 18 would therefore not be cases of APB.) The duration of the presenting symptoms in APB is very short (6 h to 4 days). It even developed in hospital and, without thiamine, the patients usually died within 48 h of admission. Sometimes no other symptom preceded the onset of breathlessness. Although the breathlessness was assumed to be due to heart failure, there was no cough, the lungs were clinically clear, and the patient was more comfortable lying downl-all of which suggests that acidosis and not pulmonary congestion was the cause of the dyspnoea. Platt2 was not convinced that heart failure was always the cause of death in APB, and the absence of a diuresis in some treated cases supports this point of view. The often-quoted lurid description of the disorder’ is at odds with its undramatic onset and development in SIR,-I would
not
some cases.
My error was to believe that there was a severe degree of thiamine deficiency present in this fulminating disease. While the pathogenesis of APB is not understood, it appears to be due, not to the degree of thiamine deficiency, but to other factors relating to the patient’s metabolism.],3 In a state of thiamine deficiency and, in the presence of such factors, a sudden excess carbohydrate intake may precipitate or worsen beriberi, resulting in encephalopathy, heart cannot be a failure, paralysis, and presumably APB. The deficiency 5
5 mg of thiamine will cure APB/ My paper (Aug 25, p 446) and the above comments raise the question as to whether "spontaneous type B lacticacidosis" exists as an entity or syndrome apart from APB. Was APB adequately excluded by Huckabee when he described the new Most of his nine patients died within 48 h of onset of the hyperpnoea. The patients were receiving hospital diets and vitamin supplements and, at onset, no evidence of heart failure was present. At first this would seem to exclude APB as a cause of the lacticacidosis, except that we know that the absorption of thiamine may be impaired and that beriberi may develop during convalescence. Huckabee also laid great stress on the presence of an increased lactate-pyruvate ratio, but an increased lactate-pyruvate ratio also occurs in APB. 6,7
8
Cubberley PT, Polster SA, Schulman CL Lactic acidosis and death after the treatment of obesity by fasting N Engl J Med 1965, 272: 628-30.
9 Oliva
PB, Schwartz HA. Survival of a patient with spontaneous lactic acidosis Ann Intern Med 1969, 71: 587-91
ONCE-DAILY ANTIBIOTIC TREATMENT OF CAPD PERITONITIS
SIR,-Peritonitis remains the main threat to successful ambulatory peritoneal dialysis (CAPD). We have to attempted develop a treatment policy that has a sound microbiological base, but which can be used easily by the patient treating himself at home. A study of the antibiotic sensitivities of organisms isolated from infected dialysis specimens over one year
continuous
showed that the most reliable initial treatment would be a combination of vancomycin and an aminoglycoside. The treatment policy adopted was as follows. After samples of dialysate fluid have been taken for microscopy and culture, 100 mg vancomycin and 40 mg gentamicin are added to the next bag of dialysis fluid. Patients who are not seriously ill are then allowed home with instructions to add 100 mg vancomycin and 40 mg gentamicin to subsequent overnight bags only. When the results of culture are known (generally after 48 h), it is usually possible to continue with one antibiotic only. Treatment is continued for 10 days. Patients with significant systemic evidence of infection are also given an initial intravenous dose of vancomycin 500 mg and gentamicin 40 mg. Results of treatment of the first 100 consecutive episodes were: -
.BafMr;0/0!t:a//!M!M; Culture positive episodes Gram-positive strains(100% vancomycinsensitive) Gram-negative strains (66% gentamicin sensitive)
No 83 74 18
Cure achieved with-
Once-daily treatment only Extended course of vancomycin Other antibiotics After catheter removal
major one since
Hontelliospital treatment Episode treated entirely at home Overnight stay only Admission because of peritonitis
syndrome?4.5
Admission for other reasons
88 4 6 2 79 7 8 6
Most
patients successfully treated themselves at home without altering their dialysis routme. Only two patients required a temporary removal of the peritoneal catheter. No clinical sideeffects of the antibiotics were seen. Peak serum levels were 5 - 5 to 12 mg/1 for vancomycin and less than 3 mg/1 for gentamicin. The adoption of this policy has greatly simplified our treatment of peritonitis, increasing our cure rate and decreasing the incidence of
Although
this patient had mild mitral regurgitation there seems think this was other than a "sudden death" from asthma. Her variable airways obstruction had always responded to treatment previously when she sought medical help. It is felt this patient had inappropriate expectations of relief from repeated nebulised salbutamol when in fact she had become bronchodilator resistant. Nebulisers merely provide an alternative method of administering aerosol bronchodilator in much larger doses than the standardised pressurised aerosols. If airways do not respond additional treatment and admission to hospital are urgently needed. Her death is all the more disappointing since she had received and seemed to understand full instructions from her general practitioner about the dangers of nebuliser therapy. She had been given contingency instructions but for reasons that we shall never know she failed to comply with them. Patients with acute severe asthma who delay calling for medical assistance after a standard dose of nebulised bronchodilator has not given the expected relief are at risk of death from their disease. no reason to
The only certain way to exclude thiamine deficiency as a cause of a patient’s acute illness is not by the dietary history or even by estimation of the red blood cell transketolase activity but by the lack of response to an intravenous injection of thiamine. Was this test done in Huckabee’s cases? Another case of spontaneous lacticacidosis may have been a case of APB8 while there is doubt about the aetiology of a second case because of the apparent 9 response to intravenous methylene-blue.9 The Hospital, Alice Springs
New Territory 5750, Australia
I. S. PETHERAM
Newport
D.
F. JONES
LACTICACIDOSIS AND THIAMINE DEFICIENCY
Langen CD, Lichtenstein A. A clinical text-book of tropical medicine. Batavia Amsterdam: G Kolff, 1936: 393-421 Platt BS. Thiamine deficiency in human beriberi and in Wernicke’s encephalopathy In. Wolstenholme GEW, O’Connor M eds. Thiamine deficiency: Biochemical lesions and their clinical significance London J & A Churchill, 1967; 135-45 Platt BS Biochemical changes, especially of pyruvic acid, in relation to some clinical features of beriberi Trans Roy Soc Trop Med Hyg 1938; 31: 493-501 Huckabee WE Abnormal resting blood lactate I: the significance of hyperlactatemia in hospitalized patients. Am J Med 1961; 30: 833-39 Huckabee WE. Abnormal resting blood lactate II Lactic acidosis. Am J Med 1961; 30: 840-48. King JF, Easton R, Dunn M Acute pernicious beriberi heart disease. Chest 1972, 61:
1. De 2
3. 4
5.
Newport Chest Clinic, Newport, Gwent, NPT 4GA
CHARLES H. CAMPBELL
6.
512-14 7 Fond B, Richard C, Comoy E, Tillement JP, Auzepy P Two cases of shoshin beri beri with hemodynamic and plasma catecholamine data Intensive Care Med 1980, 6:
193-98.
regard the patients with acute pernicious beriberi (APB) as cases of hepatorenal syndrome, as Dr Anderson (Sept 15, p 644) suggests. Only one patient (case 18) was in liver failure and there are valid explanations for the renal failure of APB other than severe liver disease. The compensatory respiratory alkalosis to which Dr Hoorntje and Dr Hillen (Oct 6, p 807) draw our attention highlights the extreme hyperpnoea and the dyspnoea which are the dominant sign and the commonest symptom of APB. Even though lactic acid may accumulate in ordinary cases of beriberi heart disease and a syndrome of severe lacticacidosis, identical to APB, may complicate established beriberi, possibly the term APB should be restricted to the acute development of severe lacticacidosis in a person with no preceding symptoms of beriberi. (My cases 12, 17, 18 would therefore not be cases of APB.) The duration of the presenting symptoms in APB is very short (6 h to 4 days). It even developed in hospital and, without thiamine, the patients usually died within 48 h of admission. Sometimes no other symptom preceded the onset of breathlessness. Although the breathlessness was assumed to be due to heart failure, there was no cough, the lungs were clinically clear, and the patient was more comfortable lying downl-all of which suggests that acidosis and not pulmonary congestion was the cause of the dyspnoea. Platt2 was not convinced that heart failure was always the cause of death in APB, and the absence of a diuresis in some treated cases supports this point of view. The often-quoted lurid description of the disorder’ is at odds with its undramatic onset and development in SIR,-I would
not
some cases.
My error was to believe that there was a severe degree of thiamine deficiency present in this fulminating disease. While the pathogenesis of APB is not understood, it appears to be due, not to the degree of thiamine deficiency, but to other factors relating to the patient’s metabolism.],3 In a state of thiamine deficiency and, in the presence of such factors, a sudden excess carbohydrate intake may precipitate or worsen beriberi, resulting in encephalopathy, heart cannot be a failure, paralysis, and presumably APB. The deficiency 5
5 mg of thiamine will cure APB/ My paper (Aug 25, p 446) and the above comments raise the question as to whether "spontaneous type B lacticacidosis" exists as an entity or syndrome apart from APB. Was APB adequately excluded by Huckabee when he described the new Most of his nine patients died within 48 h of onset of the hyperpnoea. The patients were receiving hospital diets and vitamin supplements and, at onset, no evidence of heart failure was present. At first this would seem to exclude APB as a cause of the lacticacidosis, except that we know that the absorption of thiamine may be impaired and that beriberi may develop during convalescence. Huckabee also laid great stress on the presence of an increased lactate-pyruvate ratio, but an increased lactate-pyruvate ratio also occurs in APB. 6,7
8
Cubberley PT, Polster SA, Schulman CL Lactic acidosis and death after the treatment of obesity by fasting N Engl J Med 1965, 272: 628-30.
9 Oliva
PB, Schwartz HA. Survival of a patient with spontaneous lactic acidosis Ann Intern Med 1969, 71: 587-91
ONCE-DAILY ANTIBIOTIC TREATMENT OF CAPD PERITONITIS
SIR,-Peritonitis remains the main threat to successful ambulatory peritoneal dialysis (CAPD). We have to attempted develop a treatment policy that has a sound microbiological base, but which can be used easily by the patient treating himself at home. A study of the antibiotic sensitivities of organisms isolated from infected dialysis specimens over one year
continuous
showed that the most reliable initial treatment would be a combination of vancomycin and an aminoglycoside. The treatment policy adopted was as follows. After samples of dialysate fluid have been taken for microscopy and culture, 100 mg vancomycin and 40 mg gentamicin are added to the next bag of dialysis fluid. Patients who are not seriously ill are then allowed home with instructions to add 100 mg vancomycin and 40 mg gentamicin to subsequent overnight bags only. When the results of culture are known (generally after 48 h), it is usually possible to continue with one antibiotic only. Treatment is continued for 10 days. Patients with significant systemic evidence of infection are also given an initial intravenous dose of vancomycin 500 mg and gentamicin 40 mg. Results of treatment of the first 100 consecutive episodes were: -
.BafMr;0/0!t:a//!M!M; Culture positive episodes Gram-positive strains(100% vancomycinsensitive) Gram-negative strains (66% gentamicin sensitive)
No 83 74 18
Cure achieved with-
Once-daily treatment only Extended course of vancomycin Other antibiotics After catheter removal
major one since
Hontelliospital treatment Episode treated entirely at home Overnight stay only Admission because of peritonitis
syndrome?4.5
Admission for other reasons
88 4 6 2 79 7 8 6
Most
patients successfully treated themselves at home without altering their dialysis routme. Only two patients required a temporary removal of the peritoneal catheter. No clinical sideeffects of the antibiotics were seen. Peak serum levels were 5 - 5 to 12 mg/1 for vancomycin and less than 3 mg/1 for gentamicin. The adoption of this policy has greatly simplified our treatment of peritonitis, increasing our cure rate and decreasing the incidence of