WordNet

of or relating to metabolism; "metabolic rate"
undergoing metamorphosis (同)metabolous
abnormally high acidity (excess hydrogen-ion concentration) of the blood and other body tissues

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新陳代謝の
酸性症,酸中毒(血液中のアルカリ濃度が異常に低い状態)

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/02/27 07:24:27」(JST)

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In medicine, metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO₃⁻) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia.

Terminology

Acidosis refers to a process that causes a low pH in blood and tissues.
Acidemia refers specifically to a low pH in the blood.

In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed.

Signs and symptoms

Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Over compensation via respiratory alkalosis to form an alkalemia does not occur.

Extreme acidemia leads to neurological and cardiac complications:

Neurological: lethargy, stupor, coma, seizures.
Cardiac: arrhythmias (ventricular tachycardia), decreased response to epinephrine; both lead to hypotension (low blood pressure).

Physical examination occasionally reveals signs of disease, but is otherwise normal. Cranial nerve abnormalities are reported in ethylene glycol poisoning, and retinal edema can be a sign of methanol (methyl alcohol) intoxication. Longstanding chronic metabolic acidosis leads to osteoporosis and can cause fractures.

Diagnosis

Arterial blood gas sampling is essential for the diagnosis. If the pH is low (under 7.35) and the bicarbonate levels are decreased (<24 mmol/l), metabolic acidemia is present, and metabolic acidosis is presumed. Due to respiratory compensation (hyperventilation), carbon dioxide is decreased and conversely oxygen is increased. An ECG can be useful to anticipate cardiac complications.

Other tests that are relevant in this context are electrolytes (including chloride), glucose, renal function and a full blood count. Urinalysis can reveal acidity (salicylate poisoning) or alkalinity (renal tubular acidosis type I). In addition, it can show ketones in ketoacidosis.

To distinguish between the main types of metabolic acidosis, a clinical tool called the anion gap is considered very useful. It is calculated by subtracting the chloride and bicarbonate levels from the sodium.

Anion gap = ( [Na⁺] + [K⁺] ) − ( [Cl⁻] + [HCO₃⁻] )

As sodium is the main extracellular cation, and chloride and bicarbonate are the main anions, the result should reflect the remaining anions. Normally, this concentration is about 8-16 mmol/l (12±4). An elevated anion gap (i.e. > 16 mmol/l) can indicate particular types of metabolic acidosis, particularly certain poisons, lactate acidosis and ketoacidosis.

As the differential diagnosis is made, certain other tests may be necessary, including toxicological screening and imaging of the kidneys. It is also important to differentiate between acidosis-induced hyperventilation and asthma; otherwise, treatment could lead to inappropriate bronchodilation.[1]

Causes

Metabolic acidosis occurs when the body produces too much acid, or when the kidneys are not removing enough acid from the body. There are several types of metabolic acidosis. The main causes are best grouped by their influence on the anion gap.

It bears noting that the anion gap can be spuriously normal in sampling errors of the sodium level, e.g. in extreme hypertriglyceridemia. The anion gap can be increased due to relatively low levels of cations other than sodium and potassium (e.g. calcium or magnesium).

Increased anion gap

Causes include:

lactic acidosis
ketoacidosis
chronic renal failure (accumulation of sulfates, phosphates, urea)
intoxication:
- organic acids (salicylates, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde, INH)
- sulfates, metformin (Glucophage)
massive rhabdomyolysis

A Mnemonic can also be used - MUDPILES

M-Methanol
U-Uremia (chronic kidney failure)
D-Diabetic ketoacidosis
P-Propylene glycol ("P" used to stand for Paraldehyde but this substance is not commonly used today)
I-Infection, Iron, Isoniazid, Inborn errors of metabolism
L-Lactic acidosis
E-Ethylene glycol (Note: Ethanol is sometimes included in this mnemonic as well, although the acidosis caused by ethanol is actually primarily due to the increased production of lactic acid found in such intoxication.)
S-Salicylates

Normal anion gap

Causes include:^[1]

longstanding diarrhea (bicarbonate loss)
bicarbonate loss due to taking topiramate
pancreatic fistula
uretero-sigmoidostomy
Renal tubular acidosis (RTA)
intoxication:
- ammonium chloride
- acetazolamide (Diamox)
- bile acid sequestrants
- isopropyl alcohol
renal failure (occasionally)
inhalant abuse
toluene

Pathophysiology

Compensatory mechanisms

Metabolic acidosis is either due to increased generation of acid or an inability to generate sufficient bicarbonate. The body regulates the acidity of the blood by four buffering mechanisms.

bicarbonate buffering system
Intracellular buffering by absorption of hydrogen atoms by various molecules, including proteins, phosphates and carbonate in bone.
Respiratory compensation
Renal compensation

Buffer

The decreased bicarbonate that distinguishes metabolic acidosis is therefore due to two separate processes: the buffer (from water and carbon dioxide) and additional renal generation. The buffer reactions are:

The Henderson-Hasselbalch equation mathematically describes the relationship between blood pH and the components of the bicarbonate buffering system:

Using Henry's Law, we can say that [CO₂]=0.03xPaCO₂

(PaCO₂ is the pressure of CO₂ in arterial blood)

Adding the other normal values, we get

Treatment

A pH under 7.1 is an emergency, due to the risk of cardiac arrhythmias, and may warrant treatment with intravenous bicarbonate. Bicarbonate is given at 50-100 mmol at a time under scrupulous monitoring of the arterial blood gas readings. This intervention, however, has some serious complications in lactic acidosis and, in those cases, should be used with great care.

If the acidosis is particularly severe and/or there may be intoxication, consultation with the nephrology team is considered useful, as dialysis may clear both the intoxication and the acidosis.

References

^ MedicalMnemonics.com: 2001

UpToDate Contents

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1. 成人における代謝性アシドーシスへのアプローチ approach to the adult with metabolic acidosis
2. 代謝性アシドーシスを有する小児に対するアプローチ approach to the child with metabolic acidosis
3. 慢性腎疾患における代謝性アシドーシスの病因および治療 pathogenesis and treatment of metabolic acidosis in chronic kidney disease
4. 高アニオンギャップ性代謝性アシドーシス患者におけるΔアニオンギャップ／ΔHCO3
比 the anion gap hco3 ratio in patients with a high anion gap metabolic acidosis
5. 代謝性アシドーシスにおける尿のアニオンギャップおよび浸透圧ギャップ urine anion and osmolal gaps in metabolic acidosis

English Journal

The Effect of Osteoporosis Treatments on Fatigue Properties of Cortical Bone Tissue.

Brock GR1, Chen JT1, Ingraffea AR2, MacLeay J3, Pluhar GE4, Boskey AL5, van der Meulen MC6.
Bone reports.Bone Rep.2015 Jun 1;2:8-13.
Bisphosphonates are commonly prescribed for treatment of osteoporosis. Long-term use of bisphosphonates has been correlated to atypical femoral fractures (AFF). AFFs arise from fatigue damage to bone tissue that cannot be repaired due to pharmacologic treatments. Despite fatigue being the primary da
PMID 25642445

The efficacy and safety of entecavir in patients with chronic hepatitis B- associated liver failure: a meta-analysis.

Zhang X1, Liu L2, Zhang M1, Gao S1, Du Y1, An Y3, Chen S1.
Annals of hepatology.Ann Hepatol.2015 Mar-Apr 2015;14(2):150-160.
Background. The effectiveness of nucleoside analogue (NA) treatment in patients with chronic hepatitis B (CHB) -associated liver failure is still controversial. Severe lactic acidosis has been reported during entecavir (ETV) treatment in patients with impaired liver function. Aim. To investigate the
PMID 25671823

The effect of continuous blood purification on the prognosis of cardiorenal syndrome patients.

Jia F1, Rong P, Li D, Wang S, Jing Y, Ge Y, Meng J.
Cell biochemistry and biophysics.Cell Biochem Biophys.2015 Mar;71(2):957-61. doi: 10.1007/s12013-014-0293-x.
To discuss the effect of continuous blood purification (CBP) on the prognosis of cardiorenal syndrome (CRS) patients. Twenty-seven patients were selected for this study, who had previously been treated at the Blood Purification Center of the General Hospital of Jinan Military Region from May 2007 to
PMID 25304742

Japanese Journal

カーボスターP透析による骨のカルシウム調節能の変化について

正井基之,坂井健彦,内野順司 [他]
日本透析医学会雑誌 45(8), 635-644, 2012-08
NAID 40019426834

糖尿病腎症4期の管理 : 骨ミネラル代謝,腎性貧血,アシデミアに対する治療とエビデンス

森克仁,稲葉雅章
内分泌・糖尿病・代謝内科 34(6), 561-566, 2012-06
NAID 40019382484

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★リンクテーブル★

リンク元	「代謝性アシドーシス」
拡張検索	「hyperchloremic metabolic acidosis」
関連記事	「metabolic」「acidosis」

「代謝性アシドーシス」

Metabolic acidosis
	Davenport diagram
Classification and external resources
ICD-10	E87.2
ICD-9	276.2
DiseasesDB	92
MedlinePlus	000335
eMedicine	emerg/312 med/1458 ped/15
Patient UK	Metabolic acidosis

　　[★]

英: metabolic acidosis
関: アシドーシス、酸塩基平衡異常

酸塩基平衡異常とその代償 SP.660

	HCO3-	pCO2
呼吸性アシドーシス	↑	↑
呼吸性アルカローシス	↓	↓
代謝性アシドーシス	↓	↑
代謝性アルカローシス	↑	↓

原因

消化管からのHCO3-喪失(下痢)・腎からのHCO3-喪失(低アルドステロン症)
有機酸の蓄積(乳酸アシドーシス、糖尿病性ケトアシドーシス、腎不全)
プロトンの蓄積(尿細管アシドーシスによるH⁺排泄の障害)

アニオンギャップによる分類

a. アニオンギャップの開大するアシドーシス　有機酸の蓄積

代謝アシドーシスをきたしているとき、HCO₃^-によりH⁺を滴定するため、HCO₃^-が減少する。HCO₃^-の減少を、Cl^-ではない陰イオンが増加することで生体内の電気的中性を保つような病態ではアニオンギャップが開大する。
(病態の形成機序としては不揮発酸が増大した結果としてHCO₃^-が減少しているのだが)
(1)腎不全時のリン酸、硫酸の増加、(2)低酸素血症時の乳酸の増加[ 乳酸アシドーシス ]、(3)ケトン体増加[ 糖尿病性ケトアシドーシス ]

b. アニオンギャップの開大しない代謝性アシドーシス　プロトン過剰 or HCO3-喪失

水・電解質と酸塩基平衡改訂第2版

メカニズム：代謝アシドーシスでは、HCO₃^-によりH⁺を滴定されておりHCO₃^-が減少する。代償的にCl^-が増加してアニオンジャップが正常になっている(Cl-の値に注意する)。

(不揮発性酸の過剰産生ではなく、代謝的にHCO₃^-の過剰喪失、H⁺の過剰産生、H+の排泄障害が考えられる)

分類

HCO₃^-喪失

近位尿細管性アシドーシス：(低K血症を伴う)
ファンコニ症候群
炭酸脱水酵素阻害薬(アセタゾラミド)
副甲状腺機能亢進症：副甲状腺ホルモンは近位尿細管での重炭酸イオンの再吸収を抑える(高Cl性代謝性アシドーシス)
下痢：(低K血症を伴う)
尿管S状結腸吻合

尿細管アシドーシスによるH⁺排泄の障害

遠位尿細管性アシドーシス：(低K血症を伴う)
低アルドステロン症
アジソン病　→　高カリウム血症により尿細管上皮細胞内のH+が減少するためだっけ？
先天性副腎皮質過形成　→　高カリウム血症により尿細管上皮細胞内のH+が減少するためだっけ？

NH₄Cl負荷などの外因性H⁺摂取

症状

周期性深呼吸、脱力感、意識障害・昏睡
腎石灰化症？　→　カルシウムの排泄量が増加するため。 ex.RTA I

検査

血液ガス：pH↓
尿検査：カルシウム排泄増加　←　遠位尿細管でのカルシウム再吸収が抑制されるため。

治療

重炭酸ナトリウム投与：volume overload、イオン化カルシウムの減少によりテタニーに注意

後者は、急激にpHを上げると、アルブミンが負に帯電、イオン化カルシウムが急激に減少することでテタニーを生じる。このような場合にはグルコン酸カルシウムの投与を行う。(QB.D-354)

その他

代謝性アシドーシスでは、呼吸性代償が機能していれば、PaCO2=pHの小数点以下2桁、となる。pH 7.34の代謝性アシドーシスではPaCO2 34Torrが期待されるが、34を大きく上回る場合、呼吸性代償が機能していないと判断される。(出典不明)

「hyperchloremic metabolic acidosis」

　　[★] 高クロール性代謝性アシドーシス

「metabolic」

　　[★]

adj.

代謝性の、代謝的な、メタボリックな

関: metabolically

「acidosis」

　　[★] アシドーシス

[1] MedicalMnemonics.com: 2001

匿名

検索

案内

metabolic acidosis