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。     

传染性非典型肺炎159例酸碱平衡与临床分型及病程关系分析

目的探讨各型严重急性呼吸综合征每周的酸碱失衡情况及其规律。方法159例患者，住院后每周测定血气分析，每位患者每周只取一次血气结果，共得血气分析结果430例次，分周分型进行统计。结果发病前2周，普通型和重型患者酸碱失衡以代碱呼碱为主；而极重型以呼碱代酸为主；极重型患者第1周呼碱型三重失衡比例较多，仅次于呼碱加代酸位居第二位：第3周后，普通型患者单纯代碱的比例迅速上升并跃居首位，而重型患者则虽也上升但相对较慢，代碱呼碱仍处于首位，极重型则代碱呼碱比例上升为首位；代碱代酸而同时不合并呼吸性酸碱失衡者仅在普通型存在；呼酸比例在普通型中从第2周逐渐增多，至第5周出现高峰。结论患者病程2周内出现呼碱代酸或呼碱型三重酸碱失衡，应高度警惕发展为极重型的可能，积极加强治疗；出现单纯的代碱或排除气道阻塞、呼吸肌疲劳及机械通气因素造成的呼酸，以及呼碱消失，可能预示着病情开始恢复；应用某些药物时要随时注意酸碱失衡，及时调整或纠正；应用机械通气要着重对呼碱因素进行治疗，合理调整压力水平。     

急性脑血管病患者应激性高血糖、血清钾、钠、氯的变化及其与中风类型、病情轻重、预后关系

目的探讨急性脑血管病患者应激性高血糖、血清钾、钠、氯的变化及其与中风类型、病情轻重、预后关系。方法本文对我院神经内科2004年6月～2005年6月住院急性脑血管病患者248例进行研究，其中出血性中风89例，缺血性中风159例，于入院次日晨检测空腹血糖、血清钾、钠、氯，观察血糖、血钠、血氯、血钾值的变化及其与脑卒中类型、病情轻重、预后关系。结果（1）急性脑血管病患者易出现应激性高血糖、低钠血症、低氯血症、低钾血症；（2）出血性中风血糖明显高于缺血性中风；高血糖组死亡率明显高于非高血糖组；死亡组的血糖均值亦显著高于存活组；统计学上差异有显著性。（3）出血性中风低血钠、低血氯的发生率明显高于缺血性中风，统计学上差异有显著性；低血钠、低血氯组中的中、重度患者显著多于正常血钠、血氯组；与正常血钠、血氯组相比，高血钠、高血氯组患者在中风类型、病情轻重及预后方面差异均无显著性，但血钠、血氯显著升高时，死亡率明显增加。与正常血钾组相比，低血钾组中患者在中风类型、病情及预后方面差异无显著性，但血钾明显降低时，病死率增加。高血钾组患者在中风类型、病情轻重和正常血钾组相比差异无显著性，但病死率则明显高于正常血钾组。结论急性脑血管病患者存在应激反应，急性脑血管病患者应激性高血糖、低钠血症、低氯血症可以作为判断急性脑血管病病情、预后评估的指标之一。高钠血症、高氯血症、高钾血症、低钾血症与中风类型、病情及预后方面差异无显著性，但当出现严重的高钠血症、高氯血症、高钾血症、低钾血症时，病死率明显增加。     

酸碱失衡类型系统划分及划分视图设计

酸碱失衡类型划分在不断完善。传统的酸碱失衡类型仅有：代谢性酸中毒（代酸）、代谢性碱中毒（代碱）、呼吸性酸中毒（呼酸）、呼吸性碱中毒（呼碱）、呼酸并代酸、呼酸并代碱、呼碱并代酸、呼碱并代碱八型。随着阴离子间隙（anion gap,AG）和潜在HCO3^-（potential bicarbonate）概念在酸碱失衡领域中的应用,人们又提出了几种新的酸碱失衡类型：①高Cl-性代酸并高AG代酸;②代碱并高AG代酸;③三重酸碱失衡（triple acid—base disturbance,TABD）,包括呼酸＋代碱＋高AG代酸（呼酸型TABD）和呼碱＋代碱＋高AG代酸（呼碱型TABD）两型。     

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、ＨＣＰ３＾－值代入酸碱失衡预计偿公式,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 到碱失衡发生率,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,     

肝硬变腹水并低钠血症43例

肝硬变腹水并低钠血症４３例倪德明李铎上海市杨浦区中心医院消化内科２０００９０主题词肝硬化／并发症腹水低钠血症／病因学Ｓｕｂｊｅｃｔｈｅａｄｉｎｇｓｌｉｖｅｒｃｉｒｒｈｏｓｉｓ／ｃｏｍｐｌｉｃａｔｉｏｎｓａｓｃｉｔｅｓｈｙｐｏｎａｔｒｅｍｉａ／ｅｔ...     

三种不同方法对三重酸碱紊乱判定的比较

三种不同方法对三重酸碱紊乱判定的比较罗炎杰，肖欣荣三重酸碱紊乱（ＴＡＢＤ）是指一种呼吸性酸碱紊乱合并高阴离子间隙（ＡＧ）代酸或代碱，其中呼酸＋代酸＋代碱者为呼酸型ＴＡＢＤ，呼碱＋代酸＋代碱者为呼碱型ＴＡＢＤ。目前判定ＴＡＢＤ的方法尚不一致，判定结果差...     

ICU危重患者血气分析1696例报告

目的提高对危重患者并发酸碱失衡的认识。方法对1696例危重患者酸碱失衡类型进行分析。结果ICU科1696例危重患者动脉血气中1648例（97．17％）伴有8种类型的酸碱失衡，其中呼吸性碱中毒（呼碱）最为常见，占447（26．36％）；其它依次为：代谢性酸中毒（代酸）316例（18．60％），呼碱合并代酸258例（15．24％），呼酸合并代碱196例（11．57％），呼吸性酸中毒（呼酸）160例（9．45％），呼碱合并代谢性碱中毒（代碱）138例（8.11％），呼酸合并代酸89例（5．23％），代碱44例（2．61％）。结论危重患者原发疾病常引起呼碱或呼酸，病情的发展或不适当的治疗导致代碱，严重外伤、顽固性休克、严重低氧血症肾功能不全而引起代酸。严重的呼碱并代碱、呼酸并代酸可导致患者出现重度的碱血症、酸血症。而致患者死亡。     

肝硬变腹水合并上消化道出血

目的为了对肝硬变腹水合并上消化道出血有进一步认识，总结了近3a157例肝硬变腹水合并上消化道出血者57例及其并发症．方法根据诊断标准，经统计学卡方验证，将出血者（57例）与无出血者（100例）合并脾功能亢进、消化性溃疡、自发性腹膜炎、肝昏迷及肾功能减退进行对照．结果出血组的肾功能减退（68．4％）及肝昏迷（26．3％）发生率明显高于未出血者（19．0％和7．0％，P＜0．01）．结论肝硬变腹水出现上消化道出血者，再合并其他并发症的发生率较未出血者高为明确出血原因及部位采取相应的治疗措施，应及时进行急诊内镜检查．     

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?     

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。     

Hyponatremia in patients with ascites complicating liver cirrhosis]

Eighty unselected cases of hyponatremia complicating liver cirrhosis were analysed. Of these cases, 20 had sodium levels less than 135 mmol/L, 48 less than or equal to 130 mmol/L and 12 less than or equal to 125 mmol/L. 5 cases developed acute hyponatremic syndrome after abdominal paracentesis and high-dose of diuretics. Of these 5 cases, 1 died and 4 recovered after immediate infusion of 3% sodium chloride (200-300 ml/d intravenously for 7-10 days). Both the crystal and colloid pressure of blood determined in 10 cases were less than normal. The sodium level of the ascitic fluid determined in 5 cases was higher than that of serum. Respiratory alkalosis complicated with metabolic alkalosis or acidosis were the main features of acid-base disorders. These might be due to alkalinizing agents therapy, infection and hepato-renal syndrome. Based on these clinical studies, it was shown that paracentesis and diuretics are the main causes of acute hyponatremic syndrome, so these measures should be taken carefully in patients with hyponatremic state previously, especially in patients with poor general, hepatic and renal conditions.     

Disturbances of fluid and electrolyte balance in patients with acute stroke

Serum sodium and potassium concentrations were measured in 196 patients with acute cerebral infarction and 56 with cerebral hemorrhage. All patients were admitted within 7 days of onset and the data within 2 weeks of admission were recorded. The incidences of hypernatremia (serum Na greater than or equal to 149 mEq/l), hyponatremia (less than or equal to 134 mEq/l), hyperkalemia (serum K greater than or equal to 4.8 mEq/l) and hypokalemia (less than or equal to 3.2 mEq/l) were higher in patients with hemorrhage (18, 7, 13 and 14%, respectively) than infarction (4.5, 4.5, 11 and 6%, respectively). The incidences of hypernatremia and hyponatremia in infarction were higher in those who had cortical lesions than in those who had lesions in the basal ganglia or infratentorium. In cerebral hemorrhage, the incidence of hypernatremia was the highest in those with brain stem lesion. Hypernatremia was found in 27% of large sized hematoma, being significantly higher than that of those with medium (16%) or small (1%) hematoma. A similar tendency was also observed in hyponatremia and hyperkalemia. In elderly patients, electrolyte disturbances were more common than in young or middle-aged patients. Renal insufficiency and diabetes mellitus were frequent complications in stroke patients with hypernatremia (42 and 32%, respectively), of which 57% died within one month of admission.     

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.     

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.     

老年肺心病并发多器官功能不全综合征71例临床分析

目的探讨老年多器官功能不全综合征(MODSE)与电解质、血气分析及病死率的关系。方法分析71例老年肺心病合并MODSE的临床资料,将其分成衰竭前期组与衰竭期组,对其肺、心、肾、脑、肝等多器官功能进行评价,对其电解质、血气分析进行统计,并分析诱因构成。结果感染是MODSE的主要诱因,衰竭期组低钠血症、呼吸性酸中毒合并代谢性酸中毒、呼吸性酸中毒合并代谢性碱中毒的发生率以及2个器官功能不全病死率显著高于衰竭前期组;MODSE病死率随器官功能不全数目增多而增加。结论重视MODSE的早期预警和干预,重视MODSE的肺启动作用,可防止MODSE的发生;重视MODSE衰竭前期救治,减少功能不全器官数,才能降低病死率、改善预后。     

Acid-base disorders in hyperglycemia of insulin-dependent diabetic patients on chronic dialysis

The authors studied hyperglycemia occurring in insulin-dependent diabetic patients on chronic dialysis to determine the types of associated acid-base disorders, their treatment, and any differences from hyperglycemia in diabetic patients with intact renal function. Eighty-eight episodes of serum glucose greater than 25 mmol/L were observed, 23 in hemodialysis patients and 65 in patients on continuous peritoneal dialysis. Treatment consisted of low-dose insulin in 77 episodes and low-dose insulin plus saline in 11; no base was administered. Seventeen episodes (19%) presented with ketoacidosis. Arterial blood gas determinations were carried out at presentation in 37 of the episodes without ketoacidosis. Of these, 12 had respiratory alkalosis, six had respiratory acidosis and severe pulmonary edema, 14 had other single or mixed acid-base disorders, and only five had normal acid-base status. Insulin corrected the ketoacidosis in all instances and both pulmonary edema and respiratory acidosis in five of six instances. In eight cases metabolic alkalosis developed during treatment, without external acid loss. At the completion of treatment respiratory alkalosis was present in half the cases. No difference was noted between patients treated with hemodialysis or peritoneal dialysis. Insulin alone is sufficient for the management of hyperglycemia in dialysis patients. Certain acid-base disorders persist, but do not need further treatment. Hyperglycemia in patients on dialysis is characterized by infrequent development of metabolic acidosis and frequent presentation with respiratory alkalosis, by respiratory acidosis that is corrected by insulin, and by metabolic alkalosis developing during treatment without external cause.     

Acid-base abnormalities and liver dysfunction

In addition to the kidneys and lungs, the liver also plays an important role in the regulation of the Acid-Base Equilibrium (ABE). The involvement of the liver in the regulation of ABE is crucial because of its role in lactic acid metabolism, urea production and in protein homeostasis. The main acid-base imbalance that occurs in patients with liver cirrhosis is Respiratory Alkalosis (RAlk). Due to the fact that in these patients additional pathophysiological mechanisms that affect the ABE are present, other disorders may appear which compensate or enhance the primary disorder. Conventional ABE reading models fail to identify and assess the underlying disorders in patients with liver cirrhosis. This weakness of the classical models led to the creation of new physicochemical mathematical models that take into account all the known parameters that develop and affect the ABE. In addition to the RAlk, in patients with liver cirrhosis, metabolic alkalosis (due to hypoalbuminemia), hyponatremic metabolic acidosis, hyperchloremic metabolic acidosis, lactic acidosis and metabolic alkalosis due to urea metabolism are some of the pathophysiological mechanisms that affect the ABE.     

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.