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Reanimation - Urgencies
Metabolic disorders
Courses of Reanimation - Urgencies
 


 

Metabolic acidosis:

A- DEFINITION:

It is defined on several parameters:

• pH < 7

• Plasmatic Rate of bicarbonate < 21 mmol

• PCO2 < 38 mmHg

B - CLINICAL SIGNS:

Not very evocative.

Appear only tardily.

1) RESPIRATORY:

Dyspnea of the Küssmaul type: acceleration of the rate of respiration (polypnée).

2) NEUROLOGICAL:

Disorders of the conscience.

3) CARDIOVASCULAR:

Cardiovascular collapse in the cases of acidosis serious.

C - BIOLOGICAL SIGNS:

1) GAS OF ARTERIAL BLOOD:

Measure PCO2.

Low alkaline reserves (bicarbonates). low pH

2) BLOOD IONOGRAMME:

Anion hole: (Na+ + K+) - (Cl - HCO3-). Normal state: < 16="">

Hyperkaliemy of transfer: passage of potassium towards blood under the effect of the acidosis.

3) URINARY pH:

Allows to distinguish 2 cases:

• Normal Response of the kidney: pH < 5="">

• Abnormal Response of the kidney: pH > 5,3

D - CAUSES:

1) ACID EXCESSES Of CONTRIBUTIONS:

a) Exogenic:

Enough rare.

Intoxication, generally voluntary, by acid products.

• Drugs: Aspirine

• Ethylene glycol

• INH: antituberculeux

b) Endogenous:

Two cases:

• Acidocétose: production of acid bodies cetosic by the organization: dependent on the diabetes.

Acidocétose not diabetic: alcoholic intoxication.

• States of shock: the lactates are a product of the anaerobic metabolism.

Lactates raised in arterial blood.

Criterion of the gravity of a state of shock.

But also in cases of hepatic insufficiency serious.

2) DEFECT Of ELIMINATION Of ACIDS:

Severe renal insufficiency: important destruction of will néphrons.

Clearance lower than 20 mmol/min.

3) EXCESSES OF ALKALINE LOSSES:

a) Digestive losses:

• Digestive Dents.

• Pancréatites

• Diarrhoeas: losses rich in bicarbonates

• Laxative with the long course and strong amount

b) Renal losses:

Tubulopathies (diseases of the tubules).

Congenital diseases.

Incapacity of the tubule to reabsorb bicarbonates.

The urines will be rich in bicarbonates.

The urinary pH will be to 6 or 7.

Absorption of DIAMOX (ophthalmology): block the reabsorption of bicarbonates.

E - TREATMENT:

1) TREATMENT ETIOLOGIQUE:

Treatment of the cause of the metabolic acidosis.

It can be enough.

2) SYMPTOMATIC TREATMENT:

Consist in plugging the acids by bicarbonates:

• Molar: 84 ‰ (hyperosmotic) 84 meq/L

• Semi-molar: 42 meq/L

• Iso: 1/6 molar (isotonic compared to plasma): 14 ‰

It is about sodium bicarbonate: at the same time as bicarbonate, salt is brought.

That can have disadvantages at the cardiac level.

One can give THAM: substitute without sodium of bicarbonate.

The moderate acidosis does not require symptomatic treatment; one does not treat that the cause.

On the other hand, it is necessary for a pH < 7="">

Ideal alkaline reserve - found alkaline reserve X 0,4 times the weight of the patient.

Give the quantity of bicarbonate to be given to the patient by 12 midnight.

Not to make up the metabolic deficit too quickly.

Not more than 5 meq/h during the first 6 hours.

To supervise by gases of blood repeated.

To supervise the kaliemy: risk hypokaliemy during the compensation.

One can be brought to bring potassium.

The metabolic alcalose:

A - DEFINITION:

• pH > 7,42

• Plasmatic Bicarbonate > 26 meq/L (26 mmol/L)

Increased • PCO2: > 42 mmHg (hypoventilation)

B - CLINICAL SIGNS:

1) SIGNS NEURO-MUSCULAIRES:

• Cramps

• Convulsions

• Crises of tetany

2) CARDIOVASCULAR SIGNS:

Not very specific and observed tardily.

C - BIOLOGICAL SIGNS:

1) GIVE BY GASES OF BLOOD:

• pH > 7,42

• Plasmatic Bicarbonate > 26 meq/L (normal 22)

• PCO2 increased > 42 mmHg

2) BLOOD IONOGRAMME:

Search for associated disorders.

Hypokaliemy at once that there is alcalose. 3) URINARY pH So lower than 6, there is acidurie paradoxical.

Allows to see whether the response of the kidney is suitable.

high urinary pH; sometimes > 7.

D - ETIOLOGY:

1) EXCESSES Of ALKALINE CONTRIBUTIONS:

a) Exogenic:

Excess of dairy produce consumption: syndrome of the milk drinkers.

Gastric bandages rich in alkaline.

Fast Ringer-lactate perfusions.

b) Endogenous:

Overdose in vitamin D.

Increase the threshold of reabsorption of bicarbonates by the kidney.

2) ACID EXCESSES OF LOSSES:

a) Acid digestive losses:

Losses known-pyloriques: repeated vomiting

b) Acid renal losses:

Caused by:

• The diuretic thiazidiques ones used against hypertension

• Diurétiques of the handle: LASILIX

• Hyperaldostéronisme

• Hypercorticisme

The reabsorption of salt and acid elimination support.

3) ALCALOSES OF CONTRACTION:

Apparent Alcalose caused by a relative increase in the concentration due to a reduction in plasmatic volume.

These various phenomena do not appear that if there is a mechanism supporting the paradoxical acidurie (acids eliminated by the urines whereas he should occur the reverse).

• Hypochlorémie

• Hyponatrémie

• Hypokaliémie

• Hypercalcémie

If not, the alcalose corrects itself.

E - TREATMENT:

1) TREATMENT ETIOLOGIQUE:

2) SYMPTOMATIC TREATMENT:

Treatment of the above supporting mechanism.

Only one cause does not involve a paradoxical acidurie: hyperparthyroidemy.

Hypokaliémies:

A - DEFINITION:

Lower plasmatic kaliemy.

Rate < 3

B - CAUSES:

1) DEPRIVE CONTRIBUTION:

• Prone old

• Large dénutris

2) INCREASE IN THE INTRACELLULAR TRANSFER:

a) Alcaloses hypokaliemic:

b) Drugs:

Kaliurétiques: diuretic which makes eliminate from potassium.

Certain products used in anaesthesia.

Insulin: to supervise the kaliemy.

c) toxic Agents:

d) Periodic paralysis:

Great accesses of severe hypokaliemy.

Periodic family disease.

Appears by generalized muscular paralyses.

3) HYPOKALIEMIES OF DEPLESSION:

Most frequent.

a) Digestive losses:

Response of the kidney which causes a reduction in urinary potassium.

• Diarrhoeas +++

• Digestive Dents

• Villous Tumours

• Laxative

b) Renal losses:

• Diurétiques +++: thiazidic, diuretic of the handle

• Tubular Acidoses: congenital tubulopathies

• Increase in the mineralocorticism: hyperaldosteronism (elimination of ions H+ and K+)

• Syndrome of Cushing

• Drugs: Ampho B, aminosides

C - CLINICAL DEMONSTRATIONS:

1) CARDIAC:

a) Anomaly with the ECG +++:

Early.

Correlated with the hypokaliemy.

Primarily disorders of the repolarisation.

b) Disorders of the rate/rhythm:

Ventricular extrasystoles.

Twists of points.

2) MUSCULAR:

a) Reduction in the muscular force:

b) Rhabdomyolyse:

Striated muscles lyse.

c) Disorders of the transit +++:

• Constipation

• Iléus

3) RENAL:

a) Polyurie:

b) Metabolic Alcalose:

One of the causes of acidurie paradoxical.

c) chronic renal Insufficiency:

Can induce it in the long run.

4) ENDOCRINE:

Associated hypoglycemia.

D - TREATMENT:

1) ETIOLOGIQUE:

2) SYMPTOMATIC:

Potassium contribution, mainly by rich foods in potassium.

But also medicamentous: syrup accompanying the treatments diuretic.

The intravenous contributions are addressed to the acute and brutal hypokaliémies.

Also if there are important cardiologic disorders: intravenous potassium injection.

Not stripped of disadvantages: poison for the veins.

Be likely to induce a hyperkaliemy.

It is recommended not to exceed a rate/rhythm of perfusion of 20 mmol/h (1 G = 13 meq = 13 mmol).

Out of peripheral, not to exceed a concentration higher than 4 g/L.

Electrocardiographic monitoring.

To supervise the kaliemy in the course of perfusion.

To avoid certain substances being able to worsen it:

• Insulin

• Diurétiques hypokaliémiants

• Digitaliques

• Quinidiniques (derivatives of quinine): cardiac toxicity.

To avoid alkalizing somebody who is in hypokaliemy.

It is not rare that a diabetic dies by induced hypokaliemy.

Hyperkaliémies:

A - PHYSIOLOGICAL RECALL:

Kaliemy > 5,5 mmol/L (K plasmatic).

There are false hyperkaliémies:

• Use of a tight garrot in way prolonged

• Hémolysés Taking away: potassium of degradation of the red globules

• Among patients having a thrombocytose: well supported hyperkaliemy

B - MECHANISMS:

1) HYPERKALIEMIE OF TRANSFER:

In the metabolic acidosises:

In the great tissue dilapidations:

• Polytraumatismes

• Rhabdomyolyse

• Destruction of the cells by a chemotherapy

2) HYPERKALIEMEIS OF OVERLOAD:

• Excess of contribution

• Defect of elimination: severe renal insufficiencies

C - CLINICAL SIGNS:

1) SIGNS ELECTRO-CARDIAQUES:

• Pointed Waves P

• Disorders of the rate/rhythm

• Brutal heart Failure

2) SIGNS NEURO-MUSCULAIRES:

Nonspecific signs: paraesthesias, paralyses.

Late signs.

D - CAUSES:

1) HYPERKALIEMIES OF TRANSFER:

• Acidosis

• Rhabdomyolyse

• Tumoral Lysis

• Drugs: digitalic, Succinyl-Choline

2) HYPERKALIEMIES OF OVERLOAD:

a) Defect of elimination:

• Acute or chronic renal Insufficiency

• Surrénalienne Insufficiency

b) Excess of contribution:

E - TREATMENT:

It is a therapeutic urgency.

One manages:

• Gluconate of calcium

• Agents b-adrenergic: 15 to 30 min

• Bicarbonate of sodium: 15 to 30 min

• Insulin IV: 15 to 30 min associated glucose

• Hemodialysis: < 30="" min="">

• Exchanging Resins of ions: 60 to 120 min (KAYEXALATE)

With this last, risks of vascular overload.

If serious:

• 2 to 3 calcium gluconate bulbs in IV slow

• Then 20 insulin UI in IVD

• 500 DC of G30 to avoid a hypoglycemia

• 40 to 100 meq of molar bicarbonated serum

In parallel, started rectal injection of KAYEXALATE: 100 G in 200 ml of water on 3 to 4 min.

Hyponatrémies:

A - GENERAL INFORMATION:

a) Definition:

Natremy < 135

Always involve an increase in intracellular volume.

Water will pass from the intravascular medium in the intracellular medium to compensate.

b) Distort hyponatrémies:

• Hyperlipidémies

• Hyperprotidémies

• Perfusion of substances osmotiquement active: DEXTRAN

• Hyperglycemia: glucose takes the place of sodium

True Natremy = calculated natremy + 1/3 of the glycemia.

B - MECHANISMS:

Three mechanisms:

a) Lower sodic capital:

Maybe owing to lack of contributions.

Maybe by excess of losses.

b) Increase in the hydrous capital:

Sodium is diluted: hyponatremy of dilution.

Most frequent.

c) Strong hypokaliémies:

Sodium replaces potassium in the cells and decreases in blood.

Rare.

C - CLINICAL SIGNS:

1) INTRACELLULAR HYPERHYDRATATION:

Involve:

• Dislike of water

• Vomiting

• Nauseas

• Obnubilation, even a coma: hyperhydratation of the cerebral cells

• Gingival Prints: left oedema of the gums

2) OTHER SIGNS:

a) Extracellular dehydration:

• Thirst

• Cutaneous Fold of dehydration

• Dryness of the mucous membranes

• Hypovolémie in the extreme cases or

b) Extracellular Hyperhydratation:

Total Hyperhydratation.

Hyponatrémies of dilution.

• Oedema

• Catch of weight

• Neurological Signs: intracranial hypertension

c) normal extracellular Hydration:

Syndrome of Schwart-Barter: inappropriate syndrome of production of ADH.

Also a hyponatremy of dilution, but moderate.

D - BIOLOGY:

Osmolarity in plasma lowered to the lower part of 280 milliosmoles.

E - ETIOLOGY:

1) HYPOONATREMIES OF DILUTION:

a) Hydrous overload:

Hydrous excesses of contributions: old people, infants, reanimation

b) Severe chronic renal insufficiency:

c) effective Hypovolémie:

Total Hypervolemy, but the plasmatic sector is depressed:

• Cirrhotiques

• Insufficient cardiac décompensés

• Syndrome nephrotic

2) HYPONATREMIE OF DEPLESSION:

Very decreased hydrous capital: generally losses

a) Renal losses:

• With salt loss

• Mineralocorticoid

• Salidiurétique

b) Extra-renal losses:

• Digestive

• Cutaneous: exposures prolonged to the sun, mucoviscidose

c) Deficiencies in contributions:

3) SYNDROME OF SCHWARTZ-BARTER:

Disordered state of the secretion of ADH:

• Lung cancer

• Acute Pneumopathies

Medicamentous •

F - TREATMENT:

a) Hydrous restriction:

b) Extra-renal purification:

By hemofiltration.

c) salt Contribution in the event of déplétion:

d) Stop of the treatment diuretic:

e) SB syndrome:

Moderate hydrous restriction.

Possible use of antagonists of the ADH.

Treatment of the subjacent cause.

Hypernatrémies:

A - DEFINITION:

Plasmatic sodium rate > 155 mmol/L.

Corollary: intracellular dehydration: salt in excess pumps the water of the cells.

B - MECHANISMS:

a) Excess of containing soda contributions:

Rare.

b) Excessive hydrous losses:

Leads to a hemoconcentration.

C - PRIVATE CLINIC:

a) Intracellular dehydration:

• Thirst

• Muqueuses dry

• Central Signs: fever, obnubilation

b) Extracellular dehydration:

• Cutaneous Fold

• Ocular Depression of the spheres

• Signs of hypovolemy: collapse

• Tachycardia

c) extracellular Hyperhydratation:

• HTA

• Signs of volemic overload

• Pulmonary or cerebral Oedema

D - BIOLOGY:

> 155 mmol/L.

Blood Osmolarity > 280.

E - ETIOLOGY:

1) HYDROUS LOSSES EXTRA-RENALES:

a) Cutaneous:

• Badly burned persons

b) Respiratory:

c) Digestive:

• Vomiting

• Diarrhoeas

• Dents

2) RENAL HYDROUS LOSSES:

a) Insipid diabetes:

Polyurie low in salt.

Insufficiency of production or action of the ADH.

• Central insipid Diabetes: defect of production

• Néphrogénique: Ineffective ADH owing to lack of receivers on the level of the kidney

b) Osmotic Polyurie:

Caused by substances osmotiquement active, for example in the event of hyperglycemia.

Perfusion of MANNITOL which involves water when it is eliminated by the kidney.

Hyperlipidemy also.

3) DEPRIVE HYDROUS CONTRIBUTIONS:

Therapeutic errors in the old men and the infants.

4) CONTAINING SODA OVERLOADS:

• Feeding-bottles rich in salt.

• Drowned out of sea water.

• Perfusion of salted serum hypertonic

F - TREATMENT:

Contribution of water low in salt.

No pure water: risk hémolyse.

Treatment of the cause.

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