Oral alkali therapy and the management of metabolic acidosis of chronic kidney disease:A narrative literature review

Chronic metabolic acidosis is a common complication seen in advanced chronic kidney disease(CKD). There is currently no consensus on its management in the Republic of Ireland. Recent trials have suggested that appropriate active management of metabolic acidosis through oral alkali therapy and modified diet can have a deterring impact on CKD progression. The potential benefits of treatment include preservation of bone health and improvement in muscle function; however,present data is limited. This review highlights the current evidence,available primarily from randomised control trials(RCTs) over the last decade,in managing the metabolic acidosis of CKD and outlines ongoing RCTs that are promising. An economic perspective is also briefly discussed to support decision-making.

Metabolic Acidosis in the Surgical Intensive Care Unit: Risk Factors, Clinical Correlates and Outcome. Findings from a High Dependency Heart and Vascular Surgical Center in Nigeria

Background: Metabolic acidosis (MA) is a common finding on the surgical ward, more so in the intensive care unit. Diseases affecting the major organ systems of the body and higher grades of surgery are common risk factors for MA. It is associated with poor treatment outcome. Aim: To determine the risk factors and clinical correlates of metabolic acidosis and assess its relationship with treatment outcome. Methodology: A retrospective study at the “Tristate Heart and vascular Center” in Ilishan-Remo South west Nigeria, on patients that had cardiac and vascular surgeries from January 2015 to December 2019. Three hundred and forty two participants took part in the study. The demographic, clinical and laboratory findings were entered. Statistical analysis was with Student’s t-test and Chi square. Results: Two hundred and six males and 136 females were studied. The incidences of metabolic acidosis prior to induction, on post-operative day one (POD1) and on POD28 were 20.7%, 39.8% and 14.1% respectively. Nine (2.6%) participants died during admission, of this, 6 (66.7%) had MA at presentation but all (100%) had MA on POD1. The Risk factors for MA were advanced age, comorbidities, open heart surgery, elevated systolic blood pressure and low eGFR. Metabolic acidosis was a risk factor for prolonged hospital stay, perioperative death and declining kidney function which was commoner among participants with preexisting kidney dysfunction. Conclusion: The incidence of metabolic acidosis was 20.7% at induction of anesthesia, rose to 39.8% on POD1 and by POD28, it has significantly reduced to 14.1%. While advancing age and comorbidities were risk factors for MA, the occurrence of MA increased the risk of declining kidney function, prolonged hospital stay and death.

Metabolic acidosis in late pregnancy due to 5-oxoproline (pyroglutamic acid)—A case report

Introduction: Accumulation of 5-oxoproline (pyroglutamic acid) is a rare cause of severe, high anion gap metabolic acidosis in adults. Case: A 21 year old lady presented at 39 weeks gestation in her first pregnancy with 2 weeks history of shortness of breath. She suffered from ear ache and had been taking Paracetamol on regular basis for a year. She was admitted to having regular alcohol intake until the pregnancy when she stopped. She was not in acute distress and all her observations were stable. The laboratory analysis of renal function was normal. Arterial blood gas showed metabolic acidosis. The anion gap 34 mEq/l which was consistent with metabolic acidosis. Plasma aminoacid screen revealed no abnormality. Chest X-rays showed patchy consolidation keeping with a chest infection. Emergency caesarean section was carried out for fetal distress in first stage of labour. Urine and serum samples were taken which showed an increase in the serum level five Oxoproline to creatinine ratio indicating pyroglutamic metabolic acidosis. Polyglutamate was found in the urine She was admitted to intensive care unit;cardiovascular stable, had no signs of sepsis. She underwent ventilation and haemofiltration. On second day of admission metabolic acidosis was corrected. During the 48 hours treatment with supportive therapy produced general overall improvement. Discussion: Metabolic acidosis that caused by 5-oxoproline results from disruption of the gamma glutamyl cycle. Glutamile synthetase (GS) deficiency is an autosomol recessive disorder. With GS deficiency, reduced glutathione levels increase gamma glutamile synthetase activity, and the resulting gamma—glutamile cystine levels are particularly converted to 5-oxoproline. Intoxication of organic acids is a differential diagnosis of high anion gap metabolic acidosis with no renal impairment, there was no evidence of ethanol, methanol or ethylene glycol ingestion. Suspicion for 5-oxoproline-associated high anion gap metabolic acidosis should be entertained when the cause of high anion gap metabolic acidosis remains poorly defined, the anion gap cannot be explained reasonably by measured organic acids, and there is concomitant acetaminophen use. Conclusion: Clinicians need to be aware of this unusual cause of anion gap acidosis because it may be more common than expected, early discontinuation of the offending agent is therapeutic, and administration of N-acetylcysteine could be beneficial.

Pyruvate is a prospective alkalizer to correct hypoxic lactic acidosis

Type A lactic acidosis resulted from hypoxic mitochondrial dysfunction is an independent predictor of mortality for critically ill patients. However, current therapeutic agents are still in shortage and can even be harmful. This paper reviewed data regarding lactic acidosis treatment and recommended that pyruvate might be a potential alkalizer to correct type A lactic acidosis in future clinical practice. Pyruvate is a key energy metabolic substrate and a pyruvate dehydrogenase(PDH) activator with several unique beneficial biological properties, including anti-oxidant and antiinflammatory effects and the ability to activate the hypoxia-inducible factor-1(HIF-1α)-erythropoietin(EPO) signal pathway. Pyruvate preserves glucose metabolism and cellular energetics better than bicarbonate, lactate, acetate and malate in the efficient correction of hypoxic lactic acidosis and shows few side effects. Therefore, application of pyruvate may be promising and safe as a novel therapeutic strategy in hypoxic lactic acidosis correction accompanied with multi-organ protection in critical care patients.

Effects of diabetic ketoacidosis in the respiratory system

Diabetes affects approximately 30 million persons in the United States. Diabetes ketoacidosis is one of the most serious and acute complications of diabetes. At the time of presentation and during treatment of diabetic ketoacidosis(DKA), several metabolic and electrolyte derangements can ultimately result in respiratory compromise. Most commonly, hypokalemia, hypomagnesemia and hypophosphatemia can eventually lead to respiratory muscles failure.Furthermore, tachypnea, hyperpnea and more severely, Kussmaul breathing pattern can develop. Also, hydrostatic and non-hydrostatic pulmonary edema can occur secondary to volume shifts into the extracellular space and secondary to increased permeability of the pulmonary capillaries. The presence of respiratory failure in patients with DKA is associated with higher morbidity and mortality. Being familiar with the causes of respiratory compromise in DKA, and how to treat them, may represent better outcomes for patients with DKA.

Euglycemic diabetic ketoacidosis:A missed diagnosis

Euglycemic diabetic ketoacidosis(DKA)is an acute life-threatening metabolic emergency characterized by ketoacidosis and relatively lower blood glucose(less than 11 mmol/L).The absence of hyperglycemia is a conundrum for physicians in the emergency department and intensive care units;it may delay diagnosis and treatment causing worse outcomes.Euglycemic DKA is an uncommon diagnosis but can occur in patients with type 1 or type 2 diabetes mellitus.With the addition of sodium/glucose cotransporter-2 inhibitors in diabetes mellitus management,euglycemic DKA incidence has increased.The other causes of euglycemic DKA include pregnancy,fasting,bariatric surgery,gastroparesis,insulin pump failure,cocaine intoxication,chronic liver disease and glycogen storage disease.The pathophysiology of euglycemic DKA involves a relative or absolute carbohydrate deficit,milder degree of insulin deficiency or resistance and increased glucagon/insulin ratio.Euglycemic DKA is a diagnosis of exclusion and should be considered in the differential diagnosis of a sick patient with a history of diabetes mellitus despite lower blood glucose or absent urine ketones.The diagnostic workup includes arterial blood gas for metabolic acidosis,serum ketones and exclusion of other causes of high anion gap metabolic acidosis.Euglycemic DKA treatment is on the same principles as for DKA with correction of dehydration,electrolytes deficit and insulin replacement.The dextrosecontaining fluids should accompany intravenous insulin to correct metabolic acidosis,ketonemia and to avoid hypoglycemia.

Ketogenic diet versus ketoacidosis： what determines the influence of ketone bodies on neurons？

Glucose is the main energy substrate for neurons, however, at certain conditions, e.g. in starvation, these cells could also use ketone bodies. This approach is used in clinical conditions as the ketogenic diet. The ketogenic diet is actually a biochemical model of fasting. It includes replacing carbohydrates by fats in daily meal. Synthesis of ketone bodies β-hydroxubutirate, acetoacetate and acetone begins once glycogen stores have depleted in the liver. The ketogenic diet can be used to treat clinical conditions, primarily epilepsy. The mechanism of neuroprotective action of ketogenic diet is not very clear. It is shown that ketone bodies influence neurons at three different levels, namely, metabolic, signaling and epigenetic levels. Ketone bodies are not always neuroprotective. Sometimes they can be toxic for the brain. Ketoacidosis which is a very dangerous complication of diabetes mellitus or alcoholism can be taken as an example. The exact mechanism of how neuroprotective properties of ketone bodies reverse to neurotoxic is yet to be established.

Overlap of diabetic ketoacidosis and hyperosmolar hyperglycemic state

Diabetic ketoacidosis(DKA)and hyperosmolar hyperglycemia state(HHS)are two life-threatening metabolic complications of diabetes that significantly increase mortality and morbidity.Despite major advances,reaching a uniform consensus regarding the diagnostic criteria and treatment of both conditions has been challenging.A significant overlap between these two extremes of the hyperglycemic crisis spectrum poses an additional hurdle.It has well been noted that a complete biochemical and clinical patient evaluation with timely diagnosis and treatment is vital for symptom resolution.Worldwide,there is a lack of large-scale studies that help define how hyperglycemic crises should be managed.This article will provide a comprehensive review of the pathophysiology,diagnosis,and management of DKA-HHS overlap.

Renal calcification in children with renal tubular acidosis:What a paediatrician should know

Renal tubular acidosis(RTA)can lead to renal calcification in children,which can cause various complications and impair renal function.This review provides pediatricians with a comprehensive understanding of the relationship between RTA and renal calcification,highlighting essential aspects for clinical manage-ment.The article analyzed relevant studies to explore the prevalence,risk factors,underlying mechanisms,and clinical implications of renal calcification in children with RTA.Results show that distal RTA(type 1)is particularly associated with nephrocalcinosis,which presents a higher risk of renal calcification.However,there are limitations to the existing literature,including a small number of studies,heterogeneity in methodologies,and potential publication bias.Longitudinal data and control groups are also lacking,which limits our understanding of longterm outcomes and optimal management strategies for children with RTA and renal calcification.Pediatricians play a crucial role in the early diagnosis and management of RTA to mitigate the risk of renal calcification and associated complications.In addition,alkaline therapy remains a cornerstone in the treatment of RTA,aimed at correcting the acid-base imbalance and reducing the formation of kidney stones.Therefore,early diagnosis and appropriate therapeutic interventions are paramount in preventing and managing renal calcification to preserve renal function and improve long-term outcomes for affected children.Further research with larger sample sizes and rigorous methodologies is needed to optimize the clinical approach to renal calcification in the context of RTA in the pediatric population.

106例HIV合并马尔尼菲篮状菌感染特征及预后不良相关因素分析

目的分析HIV合并马尔尼菲篮状菌感染特征及预后不良相关因素。方法回顾性分析河池市人民医院2020年2月—2023年12月106例HIV合并马尔尼菲篮状菌病的一般人口特征、合并症与预后的相关性。结果壮族与其他民族在HIV-TSM感染恶化进展上有统计学差异(P<0.05)。合并症中脓毒血症、代谢性酸中毒、血小板减少在好转组和恶化组的构成比中有显著性统计学差异(P<0.001);采用单因素Cox比例风险回归分析中代谢性酸中毒、血小板减少、脓毒血症与恶化特征有相关性;多因素Cox比例风险回归分析血小板减少是恶化的独立风险因素(HR=2.955,95%CI=1.304~6.699;P=0.009),代谢性酸中毒是恶化的独立风险因素(HR=6.219,95%CI=2.740~14.116;P<0.001)。Kaplan-Meier分析提示血小板减少与HIV-TSM恶化预后相关(Log-Rand,χ^(2)=11.511,P<0.001),代谢性酸中毒与HIV-TSM恶化预后相关(Log-Rand,χ^(2)=44.847,P<0.001);受试者工作特征曲线分析血小板减少联合代谢性酸中毒AUC为0.794(P<0.001,95%CI:0.690~0.892)。结论广西西北部壮族人群与其他民族相比在HIV-TSM感染预后不良上具有统计学差异,血小板减少和代谢性酸中毒是HIV-TSM感染预后不佳的独立风险因素。

血清碳酸氢盐水平与腹膜透析患者心血管事件关联性研究

目的 探讨血清碳酸氢盐水平与腹膜透析(PD)患者心血管事件的关联性。方法 回顾性收集行PD置管术并规律随访至2023年3月31日的PD患者资料,根据时间平均血清碳酸氢盐水平将纳入患者分为低碳酸氢盐组和正常碳酸氢盐组,比较两组患者心血管事件(包括冠心病、心力衰竭、卒中、外周血管疾病、与心血管手术相关的死亡或动脉瘤夹层或破裂导致的死亡、致命性肺栓塞或由于其他或未知的心血管原因导致的死亡)的发生率以及分析发生心血管事件的危险因素。结果 截止随访时共纳入PD患者110例,出现心血管事件34例,与正常碳酸氢盐组相比,低碳酸氢盐组患者的心血管事件发生率更高。单因素Cox回归分析表明,低碳酸氢盐组是正常碳酸氢盐组发生心血管事件风险的4.197倍(95%CI=2.115~8.331,P<0.001),校正多种混杂因素后显示低碳酸氢盐组是正常碳酸氢盐组发生心血管事件风险的3.506倍(95%CI=1.709~7.193,P=0.001)。多因素竞争风险模型结果显示,低碳酸氢盐组是正常碳酸氢盐组发生心血管事件风险的3.801倍(95%CI=1.920~7.525,P<0.001)。结论 低血清碳酸氢盐水平与PD患者发生心血管事件密切相关,是PD患者发生心血管事件的独立危险因素。

Methylmalonic Acidemia: An Unusual Cause of Chronic Renal Disease in Adults

Background: Methylmalonic aciduria (MMA) is a genetic disorder of aminoacid metabolism, due to mutations in methylmalonyl-CoA mutase, which leads to the accumulation of methylmalonic acid in body fluids. Patients typically present at the age of 1 month to 1 year with dehydration, renal impairment as well as neurologic manifestations viz. seizure, encephalopathy, strokes and disease in the globus pallidi. The case: a 26-year-old man presented with severe acute on top of chronic renal disease with serum creatinine at 590 umol/L and bilateral 8 cm kidneys with thin and echogenic cortex. He had: (a) hypernatremic dehydration, metabolic acidosis and high ammonia level with (b) a history of multiple similar attacks since the age of 8 months. Diagnosis of MMA was confirmed by high serum and urine enzymatic levels as well as genetic testing. His initial management included support with replacements of fluids, electrolytes, and bicarbonates as well as intravenous dextrose, vitamin B12 and broad-spectrum antibiotic (Meropenem) for his chest infection. Subsequently, he received 1) CARBAGLU (carglumic acid) for 7 days to lower his ammonia level to Conclusion: Untreated homozygous MMA variants, can achieve adulthood with significant renal disease yet their morbidity and mortality can be ameliorated with diet and specific therapy.

1例阿莫西林致严重代谢性酸中毒合并高乳酸血症继发急性肾损伤分析

目的分析1例女性患者口服阿莫西林后出现严重代谢性酸中毒合并高乳酸血症继发急性肾损伤案例,为临床用药提供参考。方法对该患者临床特点、相关检查,治疗方案进行回顾,并提出用药建议。结果患者口服阿莫西林(2 g)1 d后出现精神状态改变,进行性加重,意识障碍,血气分析提示严重代谢性酸中毒合并高乳酸血症。依据诺氏药物不良反应评分为6分(很可能相关),即该患者严重代谢性酸中毒和高乳酸血症“很可能”由口服阿莫西林胶囊所致,急性肾损伤继发于严重酸中毒。经过治理患者病情迅速逆转,住院1周出院。结论接受阿莫西林治疗患者出现不能解释的病情变化时,需立即完善相关检查,排除严重代谢性酸中毒、肾衰竭等危及生命的不良反应。对于阿莫西林相关严重代谢性酸中毒,需充分评估,必要时启动连续性血液净化治疗,防止病情进一步恶化,改善预后。

氨甲环酸联合碳酸氢钠注射液+林格氏液对创伤失血性休克合并创伤性凝血病患者的影响

目的:探究氨甲环酸联合碳酸氢钠注射液+林格氏液对创伤失血性休克合并创伤性凝血病患者的影响。方法:选取2022年5月—2023年2月昆明医科大学附属红河医院急诊科收治的67例创伤失血性休克合并创伤性凝血病患者作为研究对象,根据入院时间分为两组,2022年5—10月入院的33例纳入对照组,2022年11月—2023年2月入院的34例纳入观察组。两组均给予氨甲环酸和限制性液体复苏,对照组采用醋酸钠林格氏液复苏,观察组采用碳酸氢钠注射液+林格氏液复苏。比较两组氧代谢指标[静脉血氧饱和度(SvO_(2))、氧消耗(VO_(2))和氧输送(DO_(2))]、昏迷程度[格拉斯哥昏迷量表(GCS)]、休克指数、炎症因子[肿瘤坏死因子-α(TNF-α)、白细胞介素-10(IL-10)、白细胞介素-6(IL-6)]、凝血功能[活化部分凝血活酶时间(APTT)、凝血酶时间(TT)、凝血酶原时间(PT)]及并发症。结果:两组复苏前氧代谢指标、昏迷程度、休克指数、炎症因子、凝血功能比较,差异无统计学意义(P>0.05);观察组复苏后2 h SvO_(2)、VO_(2)、DO_(2)水平、GCS评分较对照组更高,休克指数及TNF-α、IL-10、IL-6水平较对照组更低,APTT、TT、PT较对照组更短,差异有统计学意义(P<0.05)。观察组并发症总发生率较对照组更低,差异有统计学意义(P<0.05)。结论:氨甲环酸联合碳酸氢钠注射液+林格氏液可以减轻创伤失血性休克合并创伤性凝血病炎症状态,提高氧代谢,改变凝血功能指标,进而提升复苏效果,减轻昏迷程度,降低相关并发症发生率。

阿德福韦酯致Fanconi综合征和低磷性骨软化症并进行性肌无力1例

阿德福韦酯是一种常用的治疗慢性乙型病毒性肝炎的药物。阿德福韦酯的肾毒性具有剂量和时间相关性,多见于30 mg/d以上剂量以及有基础肾功能损害的患者。我们报道1例慢性乙肝患者,服用阿德福韦酯10 mg/d共4年,以腰骶部和膝、髋关节疼痛为主诉就诊,曾辗转多家医院均误诊为强直性脊柱炎或脊柱关节病,最终确诊为获得性Fanconi综合征和低磷性骨软化症伴进行性肌无力,查阅国内外文献,类似报道不足10例,阿德福韦酯的肾损害应引起临床医师的重视。

维持性血液透析患者代谢性酸中毒对钙磷代谢的影响

目的:分析比较维持性血液透析(MHD)患者的代谢性酸中毒对钙磷代谢的影响。方法:选择MHD患者120例,测定透析前碳酸氢根(HCO3-)、血尿素氮(BUN)、肌酐(CR)、钙(Ca)、磷(P)、碱性磷酸酶(ALP)、甲状旁腺激素(iPTH)及透析后BUN和CR,计算钙磷乘积(Ca×P)、Kt/V。根据HCO3-分为3组:A组(HCO3-<20mmol/L)、B组(HCO3-为20～24mmol/L)和C组(HCO3-≥24mmol/L),比较3组酸中毒对钙磷紊乱的影响。结果:B、C组的P、ALP及iPTH均低于A组(P<0.05),C组的P、Ca×P低于A、B组(P<0.05)。HCO3-浓度与P、iPTH、ALP及Ca×P呈负相关(P<0.05)。结论:对于MHD患者,HCO3-<20mmol/L较HCO3-≥20mmol/L者易合并高磷血症、低钙血症,可刺激iPTH的合成,最终导致肾性骨病及转移性钙化。

代谢性酸中毒对慢性肾衰患者血清瘦素水平的影响

目的 :初步探讨慢性肾功能衰竭 (CRF)患者血清瘦素浓度的变化与代谢性酸中毒之间的关系。 方法 :采用放射免疫分析法测定血清瘦素水平 ,观察代谢性酸中毒纠正前后CRF患者血清瘦素浓度的变化。 结果 :正常人血清瘦素浓度为 10 0± 7 0 0 μg/L。CRF代谢性酸中毒患者血清瘦素浓度于纠酸前、纠酸后即刻和纠酸后 3天分别为 14 5± 9 2 7、15 3± 11 9、19 3± 14 6 μg/L ,纠酸前、纠酸后即刻血清瘦素水平与正常对照组无明显差别 ,纠酸后 3天血清瘦素浓度较纠酸前及正常对照组明显升高 (P <0 0 1)。两组血清瘦素浓度与体重指数 (BMI)均呈明显正相关 ,且女性血清瘦素浓度均分别高于男性 (P <0 0 1)。 结论 :①本研究提示 ,代谢性酸中毒可能对体内瘦素分泌具有抑制作用 ,且CRF患者的高瘦素血症很可能在某种程度上被酸中毒所掩盖。②CRF代谢性酸中毒患者中 ,女性血清瘦素水平明显高于男性。

代偿性酸中毒、炎性反应和病因是影响急性肾损伤预后的重要因素

目的分析影响急性贤损伤(AKI)预后的因素,评判不同病因对预后的影响。方法回顾性分析507例AKI病例,分为预后良好组和预后不良组,收集临床资料,根据治疗前后SCr变化,分析AKI预后的危险因素和病因对预后的影响。结果预后良好组253例(49.9%),预后不良组254例(50.1%)。预后不良组年龄较大(P<0.001),SCr基线值较高(P<0.01),贫血和低白蛋白血症的发生率较高(P<0.01和P<0.001),炎性指标更高(P<0.001)。通过Logistic回归分析建立预后模型,分析结果显示,即使代谢性酸中毒处于HCO3-降低而p H值正常的阶段,仍是影响预后的危险因素(P<0.05),MODS(P<0.001)、炎性因子(P<0.01)和少尿(P<0.01)也是影响预后的危险因素;血白蛋白(P<0.01)和血红蛋白(P<0.05)是预后的保护性因素。本研究中,AKIN 1、2期中最常见病因为重症感染导致的AKI,AKIN 3期中最常见小管间质损害,不同分期对预后的影响无显著差别。结论 1)代偿性酸中毒、MODS、炎性反应和少尿是AKI预后的危险因素;2)需重视病因对AKI临床结局的影响。

老年急性肾衰竭患者临床特点分析

目的总结急性肾衰竭（acuterenal failure，ARF）的临床特点及不同年龄段患者的差别。方法回顾性分析507例临床、资料完整的ARF病例，按年龄分组，分析ARF的临床特点及不同年龄段患者的差别。结果年轻组146例（28．8％），中年组172例（33．9％），老年组189例（37．3％）。①病因方面，老年组以肾前性因素为主，年轻组以肾性因素为主。不同年龄组在高血压（χ^2=86．804，P〈0．001）、糖尿病（χ^2=30．163，P〈0．001）、冠心病（χ^2=70．752，P〈0．001）、心力衰竭（χ^2=13．494，P=0．001）脑血管病（χ^2=31．387，P〈0．001）等基础疾病的发病率存在显著差别，老年患者发生比例居首位。②并发症方面，不同年龄组酸中毒的发生率存在显著差异（χ^2=10．393，P=0．006），老年组更易发生。③不同年龄组的死亡（χ^2=54．835，P〈0．001）、多脏器功能障碍（mulitiple organ dysfunction syndrome, MODS）（χ^2=31．061，P〈0．001）、心功能障碍（χ^2=32．593，P〈0．001）和肺功能障碍（χ^2=15．447，P〈0．001）的发生率有显著差别，老年患者居首位。④通过Logistic回归分析建立预后模型表明：即使代谢性酸中毒处于HCO3^-降低而pH值正常的阶段，仍是影响预后的危险因素（OR2．636，95％CI1．232-5．639，P=0．013），MODS（OR28．23695％CI14．946～53．344，P〈0．001）和少尿（OR2．269，95％CI1．263-4．075，P=0．006）也是影响预后的危险因素；血白蛋白（OR0．936，95％CI0．899-0．975，P=0.001）是预后的保护性因素。结论①老年患者基础肾功能差，基础疾病多，ARF病因有别于非老年患者，以肾前性为主；②老年患者ARF发生后，酸中毒、脏器衰竭的发生率和死亡率高于非老年患者。

重症肺炎死亡患者的早期临床特征及死亡预测因素分析

目的了解重症肺炎死亡患者的临床特点,探讨与死亡相关的预后因素。方法采用回顾性研究分析郑州人民医院2008年7月至2012年2月住院的125例重症肺炎的数据,对生存患者(109例)与死亡患者(16例)的临床特点进行比较。结果死亡组和生存组基础疾病数量不同,死亡组患者患有更多基础疾病(P<0.05)。死亡组患者入院时心率高于生存组患者(P<0.05)。死亡组有合并症比例及合并症数量、入院前最高体温、入院时血小板数量、动脉血pH、PaO2、HCO3-、氧合指数(PaO2/FiO2)均低于生存组患者(P均<0.05)。Logistic回归显示基础疾病数量、心率及PaO2是重症肺炎患者死亡的预测因素。结论基础疾病数量、心率及PaO2对于重症肺炎具有较高的死亡预测价值。