Acid-base disturbances in acute asthma

The clinical features, arterial blood gases, and acid-base profile were examined in 229 consecutive episodes of acute asthma in 170 patients who required hospitalization. A simple respiratory alkalosis was the most common acid-base disturbance, occurring in 48 percent of the episodes. Metabolic acidosis, either alone or as part of a mixed disturbance, was noted in 28 percent. Of 60 episodes presenting with respiratory acidosis, 37 (62 percent) had a coexistent metabolic acidosis. Metabolic acidosis was more likely to occur in male subjects and in patients with evidence of more severe airflow obstruction. Patients with metabolic acidosis had an average anion gap of 15.8 mEq/L; these patients were more hypoxemic than those without metabolic acidosis and there was a significant inverse correlation between the anion gap and the degree of hypoxemia. We conclude that metabolic acidosis is a common finding in acute, severe asthma and suggest that the pathogenesis of lactic acidosis is multifactorial and includes contributions from lactate production by respiratory muscles, tissue hypoxia, and intracellular alkalosis.     

The syndrome of alcoholic ketoacidosis

PURPOSE: To further elucidate the clinical spectrum of alcoholic ketoacidosis (AKA). PATIENTS AND METHODS: A case series of 74 patients with AKA defined as a wide anion gap metabolic acidosis unexplained by any other disorder or toxin, including any patient with a history of chronic alcohol abuse. The setting was the Medical Emergency Department at Grady Memorial Hospital in Atlanta, Georgia, a university-affiliated inner-city hospital. RESULTS: AKA is a common disorder in the emergency department, more common than previously thought. The acid-base abnormalities are more diverse than just a wide-gap metabolic acidosis and often include a concomitant metabolic alkalosis, hyperchloremic acidosis, or respiratory alkalosis. Lactic acidosis is also common. Semiquantitative serum acetoacetate levels were positive in 96% of patients. Elevated blood alcohol levels were present in two thirds of patients in whom alcohol levels were determined, and levels consistent with intoxication were seen in 40% of these patients. Electrolyte disorders including hyponatremia, hypokalemia, hypophosphatemia, hyperglycemia, hypocalcemia, and hypomagnesemia were common on presentation. The most common symptoms were nausea, vomiting, and abdominal pain. The most common physical findings were tachycardia, tachypnea, and abdominal tenderness. Altered mental status, fever, hypothermia, or other abnormal findings were uncommon and reflected other underlying processes. CONCLUSIONS: AKA is a common disorder in chronic malnourished alcoholic persons. The acid-base abnormalities reflect not only the ketoacidosis, but also associated extracellular fluid volume depletion, alcohol withdrawal, pain, sepsis, or severe liver disease. Although the pathophysiology is complex, the syndrome is rapidly reversible and has a low mortality.     

Body fluid abnormalities in severe hyperglycemia in patients on chronic dialysis: review of published reports

Reports of dialysis-associated hyperglycemia (DH) were compared to reports of diabetic ketoacidosis (DKA) and nonketotic hyperglycemia (NKH) in patients with preserved renal function. Average serum values in DH (491 observations), DKA (1036 observations), and NKH (403 observations) were as follows, respectively: glucose, 772, 649, and 961 mg/dl; sodium, 127, 134, and 149, mmol/l; and tonicity, 298, 304, and 355 mOsm/kg. Assuming that euglycemic (serum glucose, 90 mg/dl) values were the same (sodium, 140 mmol/l; tonicity, 285 mOsm/kg) for all three states, the hyperglycemic rise in the average serum tonicity value per 100-mg/dl rise in serum glucose concentration was 1.9 mOsm/kg in DH, 3.5 mOsm/kg in DKA, and 8.1 mOsm/kg in NKH. Neurological manifestations in DH patients were caused by coexisting conditions (ketoacidosis, sepsis, and neurological disease) in most instances, and by severe hypertonicity (>320 mOsm/kg), with clearing after insulin administration, in a few instances. In 148 episodes of DH corrected with insulin only, the mean increase in serum sodium per 100-mg/dl decrease in serum glucose (Delta[Na]/Delta[Glu]) was -1.61 mmol/l. In agreement with theoretical predictions, Delta[Na]/Delta[Glu] was numerically smaller in patients with edema than in those with euvolemia. The average hyperglycemic increase in extracellular volume, calculated from changes in serum sodium concentration during correction of DH using insulin alone, was 0.013 l/l per 100-mg/dl increase in serum glucose concentration. A small number of DH patients presented with pulmonary edema rectified by insulin alone. DH causes modest hypertonicity, with few patients having neurological manifestations caused usually by other coexisting conditions. In contrast to DKA or NKH, which usually presents with hypovolemia, DH causes hypervolemia manifested occasionally by pulmonary edema. Insulin is adequate treatment for DH.     

慢性肝衰竭和失代偿期肝硬化患者血气分析的变化

目的探讨慢性肝衰竭和失代偿期肝硬化患者血气分析变化的临床意义。方法回顾性分析我科收治的37例慢性肝衰竭和失代偿期肝硬化患者的血气分析资料。结果2例患者出现明显的缺氧表现,4例患者出现立位性缺氧表现,11例患者感轻度胸闷;在36例存在酸碱失衡的患者,慢性肝衰竭组存在单纯酸碱失衡9例,两重酸碱失衡10例,三重酸碱失衡2例,失代偿期肝硬化组存在单纯酸碱失衡8例,两重酸碱失衡7例。两组患者在酸碱失衡的类型方面无统计学差异;两组均以碱中毒为主。慢性肝衰竭组中比例较高的三种类型依次为呼吸性碱中毒合并代谢性酸中毒（38．1％）、呼吸性碱中毒（23．8％）和代谢性碱中毒（14．3％）,单纯性代谢性酸中毒比例最低（4．8％）。失代偿期肝硬化组中比例较高的三种类型依次为呼吸陛碱中毒（46．7％）、呼吸性碱中毒合并代谢性碱中毒（26．7％）和呼吸性碱中毒合并代谢性酸中毒（20．0％）,代谢性碱中毒比例最低（6．7％）。结论慢性肝衰竭和失代偿期肝硬化患者存在酸碱失衡和低氧血症,动态监测血气分析并及时对症治疗对此类患眷具有重要的临床意义。     

Distinctive acid-base pattern in Wernicke's encephalopathy

Wernicke's encephalopathy may result in severe morbidity and possible mortality when unrecognized. We report a distinctive acid-base pattern that has not been associated with this syndrome. This is a case series of patients with Wernicke's encephalopathy who had an arterial blood gas measurement performed on initial presentation. Exclusion criteria were patients with an unclear diagnosis of Wernicke's encephalopathy and those for whom no arterial blood gas measurement was performed. Four patients with Wernicke's encephalopathy were included in the analysis. All 4 patients exhibited an anion-gap (primary) metabolic acidosis, accompanied by a primary respiratory alkalosis. Three of 4 patients exhibited a significant lactic acidosis. None of the patients had any competing diagnoses or dysfunction to account for this acid-base pattern. Patients with Wernicke's encephalopathy may exhibit a distinctive acid-base pattern consisting of a primary metabolic acidosis in conjunction with a primary respiratory alkalosis. Observation of this acid-base disturbance should prompt clinicians to consider thiamine deficiency disorders as a possible cause.     

Effects of long-acting somatostatin analogue (Sandostatin) on manifest diabetic ketoacidosis

Insulin deficiency and counterregulatory hormone excess are the basic process in the development of diabetic ketoacidosis (DKA). Somatostatin, which suppresses the secretion of glucagon and growth hormone, has been known to attenuate the rate of gluconeogesis and ketogenesis in insulin-dependent diabetes mellitus patients. However, the therapeutic efficacy of somatostatin has not been approved to be practical in the treatment of manifest DKA. To examine the additive effect of octreotide, the synthetic long-acting somatostatin analogue SMS 201-995, to conventional treatment of manifest DKA, we compared the correction time of acidosis, ketonuria, and hyperglycemia of patients treated with an intravenous infusion of low-dose insulin (4 units per hour) plus subcutaneous injection of octreotide (50 μg every 6 hours) by low-dose insulin alone. The correction time for hyperglycemia and acidosis did not show any difference between groups (p = 0.089, p = 0.82). However, the time for disappearance of ketonuria of the octreotide-treated group (38.0 ± 32.0 h) was reduced significantly compared to other group (68.3 ± 26.0 h) (p = 0.048). These results indicated that the addition of octreotide to conventional treatment of DKA might improve the correction of ketosis, but would not allow more rapid control of acidosis and hyperglycemia in manifest DKA.     

120例重症肺结核继发感染的酸碱失衡分析

目的 分析重症肺结核继发感染的酸碱失衡情况?方法 以ABL-505血气电解质分析仪测定患者股动脉血,所得pH?PCO2?HCO-3值代入酸碱失衡预计代偿公式,首先判断出单纯型或混合型酸碱失衡,然后根据阴离子间隙判断有无三重酸碱失衡?结果 酸碱失衡发生率,单纯型>混合型>三重酸碱失衡;呼酸型>呼碱型,代酸与代碱基本相当;通过控制感染,酸碱失衡得到明显纠正?结论 重症肺结核继发感染可使肺组织严重破坏,通气与换气功能障碍,通气/血流比例失调,造成机体酸碱失衡?控制感染是治疗的关键,补充酸?碱性液体及纠正电解质紊乱是主要方法?确保机体内环境的稳定性及重要器官的供血供氧,防止出现多脏器功能衰竭?     

Acid-base state and blood oxygenation in cardiac insufficiency treated by drug agents]

The effect of different drugs on the acid-base condition and gases of arterial blood was studied by Astrup's micromethod in 124 tests in patients with circulatory insufficiency. Cardiac glycosides correct the moderate decrease in blood oxygen tension and respiratory alkalosis in patients with left-ventricular failure. Morphine has a good arresting effect in attacks of cardiac asthma and corrects or reduces the respiratory alkalosis typical of the disease but at the same time reduces the saturation of blood with oxygen. The use of oxygen together with morphine removes this unfavourable effect of the drugs. Euphylline often intensifies respiratory alkalosis, while its effect on oxygen tension in the blood and its saturation with oxygen is poorly pronounced and diversely directed. Lasics causes a favourable correcting effect on the acid-base condition and oxygenation of blood in pulmonary edema marked by metabolic acidosis.     

Diabetic ketoacidosis: new concepts and trends in pathogenesis and treatment.

New concepts concerning the pathogenesis and therapy of diabetic ketoacidosis are reviewed. The regulation of ketogenesis by intrahepatic enzymic processes and the roles of insulin deficiency or glucagon or other counterregulatory hormone excess are summarized. Major emphasis is placed on an analysis of the use of low-dose insulin regimens for the treatment of ketoacidosis. Most patients with diabetic ketoacidosis will respond to low-dose, hourly, intravenous or intramuscular regular insulin. Low doses of insulin are as effective as high doses and have fewer associated complications of hypoglycemia and hypokalemia. Phosphorus deficiency is common in diabetic ketoacidosis and hypophosphatemia usually becomes manifest within 4 to 12 h of institution of therapy. Phosphorus supplementation is now generally recommended to replete erythrocyte 2,3-diphosphoglycerate and improve oxygen delivery to tissues. Coexistent and biochemically significant lactic acidosis is a relatively infrequent complication of diabetic ketoacidosis and when present is usually due to underlying disorders associated with poor tissue perfusion.     

急性心肌梗死患者血气变化及酸碱失衡分析

目的：探讨急性心肌梗死（AMI）患者的酸碱失衡类型及临床意义。方法：回顾性分析134例AMI患者动脉血气参数（pH、PaO2、PaCO2、HCO3^-）、酸碱失衡类型和电解质资料。结果：134例患者动脉血氧分压（PaO2）〈80mmHg者72例（53％）;发生不同类型酸碱失衡113例（84％）,最常见是呼吸性碱中毒并代谢性酸中毒（呼碱代酸）,有24例（18％）,其次为呼吸性酸中毒并代谢性酸中毒（呼酸代酸）、单纯性呼碱、单纯性代酸等,单纯性酸碱失衡43例（32％）,二重性酸碱失衡64例（48％）,三重性酸碱失衡（TABD）6例（4％）。结论：AMI患者常发生低氧血症和酸碱失衡,伴有心源性休克时容易伴有代酸;严重代谢性酸中毒合并呼酸是病情严重的标志。     

Dialysis-induced respiratory acidosis

The inability to increase alveolar ventilation can lead to CO2 retention and acute respiratory acidosis in patients with ventilatory limitation. In this case, a young woman receiving maximum ventilatory support was unable to excrete excess CO2, associated with increasing dianeal concentrations of peritoneal dialysis. Since the patient's lung disease had necessitated a large amount of ventilatory support, the patient was unable to increase VE appropriately to handle excess CO2. Peritoneal dialysate was an additional source of carbohydrates. Peritoneal dialysate is an additional carbohydrate source that may result in hypercapnia and respiratory acidosis in patients with respiratory compromise. To our knowledge, this is the first case report in an adult which demonstrates that peritoneal dialysis with high glucose loads produced an acute respiratory acidosis that was reversed by decreasing the glucose concentrations in the dialysate. Excess CO2 production should be considered with respiratory disorders associated with dialysis.     

Chronische metabolische Azidose bei Niereninsuffizienz

Chronic metabolic acidosis is a common complication in patients with renal failure. Clinically it is usually recognized by severe renal failure; however, lowered pH and bicarbonate concentrations are already detectable in patients with moderate chronic kidney disease (CKD). Many systemic functions are negatively affected by metabolic acidosis, such as protein catabolism, impairment of muscle and bone metabolism, impairment of cardiac function and lower respiratory performance. Chronic metabolic acidosis is associated with an increased mortality and progression of the underlying renal disease is enhanced. Studies in patients with moderate or severe CKD demonstrate that bicarbonate substitution slows the progression of CKD. For correction of acidosis patient diet should be enriched in fruit and vegetables and contain only moderate amounts of protein. Furthermore, oral bicarbonate substitution is often needed to control acidosis; however, this treatment is associated with a significant ingestion of sodium und consecutive volume overload which may aggravate hypertension and congestive heart failure. In patients on peritoneal dialysis acidosis is generally effectively corrected via a bicarbonate containing dialysate. In contrast patients on hemodialysis often need additional oral bicarbonate substitution.     

Ketoalkalosis as a result of triple derangement of acid-base equilibrium in a diabetic patient

Summary A diabetic patient presented with weight loss, ketosis, and hyperventilation, thus mimicking the clinical picture of diabetic ketoacidosis. Laboratory investigations revealed alkalemia and a pattern consistent with a triple derangement of acid-base equilibrium: respiratory alkalosis, metabolic acidosis and metabolic alkalosis. High cortisol level suggested a genesis of ketosis different from diabetes mellitus. The patient died suddenly from acute gastrointestinal bleeding. Autopsy showed a carcinoma of the head of the pancreas with secondary portal hypertension and rupture of varices. Pulmonary micrometastases were demonstrated. It is suggested that stress hormones were the main cause of the ‘ketoalkalotic’ pattern observed.     

重型病毒性肝炎并发三重酸碱失衡及其临床意义

探讨重型病毒性肝炎合并三重酸碱失衡的发病机理及其临床意义。用阴离子间隙（AG）概念，对99例重型肝炎患者血气分析和血电解质检查进行分析。有21例（21．2％）呈三重酸碱失衡(TABD），均为呼碱型（呼碱＋代碱＋代酸），大多数由原发呼碱或代碱转为呼碱合并代碱，最后发展为TABD。比较发现，合并TABD患者其肝肾综合征、肝性脑病、自发性细菌性腹膜炎和上消化道出血的发生率显著高于单纯酸碱失衡患者，且常合并两种以上并发症处在重型肝炎病程的晚期。重型肝炎患者合并TABD是多脏器损害和多因素作用的结果。     

Metabolic acidosis in the alcoholic: A pathophysiologic approach

The purpose of this paper is to review the acid-base abnormalities in patients presenting with metabolic acidosis due to acute ethanol ingestion and to review the theoretical constraints on ethanol metabolism in the liver. Alcohol-induced acidosis is a mixed acid-base disturbance. Metabolic acidosis is due to lactic acidosis, ketoacidosis and acetic acidosis but the degree of each varies from patient to patient. Metabolic alkalosis is frequently present due to ethanol-induced vomiting. However, it could be overlooked because of an indirect loss of sodium bicarbonate (as sodium B-hydroxybutyrate in the urine). Nevertheless, the accompanying reduction in ECF volume may play an important role in the pathogenesis of alcoholic acidosis because it could lead to a relative insulin deficiency. Treatment of alcohol acidosis should include sodium, chloride, potassium, phosphorus, magnesium and thiamine replacements slong with attention to concomitant clinical problems. Unless hypoglycemia is present, glucose need not be given immediately. We feel that insulin should be withheld unless life-threatening acidemia is present or expected. Lastly, alcohol need not be detected on admission to make the diagnosis of this metabolic disturbance. However, when present, it could contribute directly to the lactic, acetic and B-hydroxybutyric acidoses. With respect to the theoretical constraints on ethanol metabolism, it appears that “overproduction” of NADH in the liver is best averted by converting ethanol to B-hydroxybutyric acid.     

Acid-base status in liver cirrhosis. Disturbances in stable, terminal and portal-caval shunted patients.

Acid-base status was determined in 86 patients with cirrhosis of the liver. Group I comprised 55 patients living more than 3 months after examination (stable). Another 18 stable patients with a surgical porta-caval shunt (p.c.a.) formed group II. Group III consisted of 12 terminal patients without p.c.a. examined within the last week of life. With respect to liver function group II was intermediate between I and III. The most common acid-base disturbance in group I was compensated respiratory alkalosis (20%) followed by compensated metabolic alkalosis (15%). 50% of group II presented compensated respiratory alkalosis. 85% of group III showed metabolic acidosis, which was compensated in only half of the patients. Respiratory alkalosis seemed more related to impairment of liver function than to portasystemic shunting. The genesis of the terminal metabolic acidosis was complex. Renal function was reduced in 92% of group III, and lactic acidosis was found in 36%. In this group hepatic function was most severely impaired, and 60% were hypotensive. These disturbances were not related to aetiology or treatment of the liver disease.     

Diabetic ketoacidosis in adults--update of an old complication

Diabetic ketoacidosis is an acute complication of Diabetes Mellitus characterized by hyperglycemia, metabolic acidosis, dehydration, and ketosis, in patients with profound insulin deficiency. It occurs predominantly in patients with type 1 diabetes and is frequently precipitated by infections, insulin withdrawal or undiagnosed type 1 diabetes. The authors review its pathophysiology, diagnostic criteria and treatment options in adults, as well as its complications.     

Equilibrium of acidifying and alkalinizing metabolic acid-base disorders in cirrhosis.

BACKGROUND AND AIMS: Conflicting results exist with regard to metabolic acid-base status in liver cirrhosis, when the classic concept of acid-base analysis is applied. The influence of the common disturbances of water, electrolytes and albumin on acid-base status in cirrhosis has not been studied. The aim of this study was to clarify acid-base status in cirrhotic patients by analyzing all parameters with possible impact on acid-base equilibrium. PATIENTS AND METHODS: Fifty stable cirrhotic patients admitted to a university hospital. Arterial acid-base status was analyzed using the principles of physical chemistry and compared with 10 healthy controls. RESULTS: Apart from mild hypoalbuminemic alkalosis, acid-base state was normal in Child-Pugh A cirrhosis. Respiratory alkalosis was the net acid-base disorder in Child-Pugh B and C cirrhosis with a normal overall metabolic acid-base state (Base excess-1.0 (-3.6 to 1.6) vs 1.1 (-0.2 to 1.1) mmol/l, P = 0.136, compared with healthy controls, median (interquartile range)). Absence of an apparent metabolic acid-base disorder was based on an equilibrium of hypoalbuminemic alkalosis and of dilutional acidosis and hyperchloremic acidosis. CONCLUSION: A balance of offsetting acidifying and alkalinizing metabolic acid-base disorders leaves the net metabolic acid-base status unchanged in cirrhosis.     

Arzneimittelassoziierte St?rungen des S?ure-Basen-Haushalts

Renal elimination of drugs and/or their metabolites may interact with different parts of the renal tubule system resulting in drug-induced acid-base disorders. Drug withdrawal or dose adjustment is the consequence. Antibiotic-related changes include many different acid-base disorders. Penicillin might cause hypokalemia, metabolic alkalosis or high-anion metabolic acidosis, aminoglycosides and tetracyclines are associated with Fanconi syndrome. Gentamicin may cause hypokalemic metabolic alkalosis together with hypomagnesemia and hypokalemia. Treatment with loop diuretics might result in hypochloremic metabolic acidosis nowadays termed chloride-depletion alkalosis for pathophysiological reasons. Using potassium-sparing diuretics, a mild hyperchloremic metabolic acidosis along with hyperkalemia has been reported. The incidence of calcium-alkali syndrome classified by the trias hypercalcemia, metabolic alkalosis and renal failure with polyuria is increasing due to the widespread use of vitamin D and calcium supplementation. Severe metabolic acidosis is associated with propofol use (propofol-related syndrome) as well as drug use containing propylene glycol (e.g. diazepam).