Acute complications of diabetes mellitus

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I- Introduction :

Diabetes is the leading cause of blindness before & rsquo; age 50 years, dialysis support for ESRD, or d & rsquo; lower limb amputation. Fifty percent of diabetics die of & rsquo; coronary insufficiency prématurée.Pourtant, a third to half of diabetes complications could be avoided

We must distinguish metabolic complications (hypoglycemic comas, hyperosmolaire, ketoacidosis and & rsquo; lactic acidosis), the complicationsmicroangiopathiques (retinopathy, nephropathy,neuropathy), and finally the macrovascular complications

II- metabolic complications :

A- Hypoglycémies :

1- Hypoglycemia diabetic insulin- :

a- Definitions :

We talk & rsquo; hypoglycemia when the glucose value is below 0,70 g / L.on identified :

Symptomatic hypoglycemia(presence of clinical manifestations), asymptomatic hypoglycemia (glucose lowering without clinical symptoms), probable symptomatic hypoglycemia (not confirmed by a glucose measurement) and finally the relative hypoglycemia (symptoms & rsquo; hypoglycemia with higher concurrent glucose 0,70 g/L).

L & rsquo; hypoglycemia is called severe when her treatment requires the & rsquo; & rsquo intervention; a third person.

b- Circumstances of occurrence :

L & rsquo; d & rsquo hypoglycemia result, a mismatch of & rsquo; insulin compared to glucose,to know :
– accidental overdose or deliberate insulin.
– insufficient d & rsquo; carbohydrate intake (insufficient food or shifted, vomiting, gastroparésie, etc.).
– excessive glucose consumption related to the & rsquo; physical activity.
– a fault against hormone-regulation (autonomic neuropathy).

c- clinical manifestations :

They are usually classified :

  • or autonomic adrenergic signs : cold sweat, palpitations, tremors, hunger.
  • neuroglucopéniques signs: impaired concentration or the & rsquo; mood, difficulties & rsquo; s speech, incoordination, diplopie, behavioral disorders. L & rsquo; hypoglycemia in this case may lead to consciousness disorders, up up & rsquo; in coma, typically stirred, accompanied by signs of & rsquo; pyramidal irritation and sometimes convulsions. L & rsquo; association with pallor and cold sweats is highly suggestive. Capillary blood glucose is in such cases usually less than 0,30 g/L.

d- Treatment :

Minor hypoglycemia are usually treated by taking 2 or 3 sugar cubes or d & rsquo; a glass of fruit juice or d & rsquo; a gel preparation containing glucose. When they occur in a context of apparent overdose of insulin or & rsquo; sustained physical activity, must complete the quick sugar made by the d & rsquo; d & rsquo a carbohydrate; slow action.

When & rsquo; there are disorders of consciousness, he must resort to intravenous glucose (30 at 50 ml of glucose solution 50 % then solute to glucose infusion 5 %). L & rsquo; the alternative is & rsquo; intramuscular or subcutaneous d & rsquo; a vial of glucagon (1 mg) that can be performed by a person informed of the & rsquo; patient's family. It is effective in the & rsquo; & rsquo absence; depletion of glycogen reserves (young, sustained physical activity).

e- Prevention of severe hypoglycemia :

All diabetic insulin-must be aware of the early clinical manifestations and circumstances of occurrence of & rsquo; hypoglycemia and have at his disposal at all times some sugar lumps.

When & rsquo; there is a significant risk of & rsquo; severe hypoglycemia, in particular due to the non-collection of hypoglycemia, must strengthen & rsquo; & rsquo autosurveillance.L; patient education plays an important role in the prevention of severe hypoglycaemia

2- Hypoglycemia the type of diabetic 2 non-insulin-treated :

The offending drugs are primarily sulfonylureas (sulfonylurées) and Glinides.

Contributing factors of these are represented by hypoglycemia :

  • l & rsquo; kidney failure, that s & rsquo; & rsquo accompanied; a reduction in & rsquo; more or less eliminating all sulfonylureas and their metabolites. L & rsquo; kidney failure also leads to decreased catabolism & rsquo; insulin ;
  • l & rsquo; liver failure, reduces the metabolism of all sulphonylurea and Glinides
  • drug interactions d & rsquo; pharmacologic or & rsquo; pharmacodynamic

Significant drug interactions involving exposure to risk d & rsquo; hypoglycaemia with sulphonylureas (SH) and repaglinide (R).

Associations against-indicated combinations not recommended Combinations requiring precautions (enhanced surveillance)
– Miconazole (systemically or gel) + SH -Gemfibrozil+ R
  • phenylbutazone + SH -Alcool + SH or R
  • Fluconazole+ Glimépiride
-Salicylés, acide to- aminosalicylic -Sulfamides antibiotics, quinolones, clarithromyicne

  • ketoconazole, fluconazole, itraconazole -Coumariniques
  • ^ blockers, IEC
  • Fibrates
  • fluoxetine, monoamine oxidase
  • Allopurinol
  • Pentoxyphilline

– Somatostatin analogues

Often for multiple reasons, Older diabetics are particularly vulnerable to severe hypoglycaemia.

The treatment of severe hypoglycemia in principle requires the & rsquo; hospital. It must take into account the speed of & rsquo; disposal of the product and / or its active metabolites may, their frequent accumulation and potentiation of & rsquo; insulin under & rsquo; effect of & rsquo; glucose administration. Convient donc de perfuser du soluté glucose in 10 % over a prolonged period, sometimes greater than 48 hours, often due to 3 or 4 L by 24 hours, by adjusting the flow rate based on the results of capillary blood glucose.

The prevention of severe hypoglycaemia guess correct patient information and / or entourage

Inform & rsquo; around the possibility of & rsquo; hypoglycemia in case of rapid change in the & rsquo; mood or behavior d & rsquo; an elderly.

B- Acidocétose :

L & rsquo; diabetic ketoacidosis is a metabolic complication involving life-threatening and occurs in over 90 % cases in the context of & rsquo; diabetes type 1, is still unknown, either to the & rsquo; & rsquo opportunity; a therapeutic break or d & rsquo; a mismatch treatment at d & rsquo; intercurrent illness.

1- pathophysiology :

L & rsquo; d & rsquo ketoacidosis results; absolute or relative deficiency of insulin leading to high blood sugar by decreasing the & rsquo; peripheral glucose utilization and increase in hepatic production. This leads to an osmotic polyuria and electrolyte loss ; extracellular dehydration triggers mechanisms & rsquo; adaptation to retain sodium in price & rsquo; a worsening of the leak potassium. The insulin deficiency and & rsquo; increase against hormone-regulation will also promote lipolysis and P-oxidation of fatty acids resulting in hepatic production of ketone bodies, acid and acetoacetic acid P-hydroxybutyric.

L & rsquo; metabolic acidosis resulting from the & rsquo; accumulation of ketone bodies is responsible d & rsquo; a transfer of potassium intracellular environment to the extracellular environment that hides the & rsquo; importance of potassium loss.

2- clinical manifestations :

L & rsquo; s & rsquo ketoacidosis; usually settles over hours, or in some cases a few days.

Clinical features :

  • overall dehydration, predominantly extracellular (fold skin, hypotension or collapse), but having an intracellular component, especially when d & rsquo; significant hyperglycemia (thirst, dry mouth, hypotonia eyeballs) ; a Kussmaul breathing, ample and noisy polypnoea frequency greater than 20 C / min, conventionally described in 4 time (crenellated) with an inspiratory pause and expiratory, but most often 2 time ;
  • a fruity smell (pippin) s & rsquo; breath ;
  • disorders of consciousness, variable depth, ranging from & rsquo; clouding up & rsquo; in a state of coma, calm, with deep tendon areflexia, and no signs of neurological or location sign & rsquo; pyramidal irritation ;
  • digestive disorders : nausea, vomiting, abdominal pain that can sometimes mimic a surgical emergency ;
  • muscle cramps ;
  • hypothermia, able to mask an infectious syndrome.

3- Additional tests :

  • capillary blood glucose (usually clearly elevated or research and glycosuria and ketone bodies in urine ;
  • arterial blood gases : metabolic acidosis with pH drop, reduction in alkaline reserve, Hypocapnia related to the & rsquo; hyperventilation ;
  • ionogramme :
  • natremia usually within normal despite losses sodées. It may be lower or higher if rarely intracellular dehydration is important. It should be borne in & rsquo; s mind that & rsquo; hyperglycemia lowers the value of serum sodium.
  • serum potassium usually normal despite the potassium losses due to the & rsquo; effect of & rsquo; acidosis. It is high in 30 % cases and rarely lowered,
  • anion gap [na + – (Cl- + HC03-)] better than 12 mEq / L in connection with the & rsquo; & rsquo accumulation; organic acids,
  • phosphoremia usually high, s & rsquo; greatly lowering being processed ;
  • urea, often high due to dehydration. L & rsquo; associated increased creatinine testify d & rsquo; a functional renal failure ;
  • ECG can highlight repolarization disorders associated with dyskaliémie, of ventricular arrhythmias, and sometimes a triggering cause for the & rsquo; ketoacidosis (myocardial infarction) ;
  • blood count : leukocytosis with neutrophilia due to dehydration and do not necessarily testifying d & rsquo; an infectious precipitating cause.

4- Treatment :

– During the accumulation phase of & rsquo; ketoacidosis, its outpatient management is possible by the & rsquo; supplementation d & rsquo; insulin associated with carbohydrate intake and proper hydration.

– Once the & rsquo; installed ketoacidosis, l & rsquo; hospitalization is required, if possible in intensive care unit if severe signs (coma, collapsed, severe acidosis [pH <7], hypokalaemia <4 mmol / L ou hypercaliemia, hyperpotassiemia >6 mmol/L).

The management has three main components :

  • the correction of dehydration involves isotonic saline (9 g/L), usually due 1 L during the first hour, then 0,5 L / h the 4 following hours. The fluid intake are then reduced 1 L / 6 hours until & rsquo; correction of ketosis and recovery of & rsquo; feed.
  • l & rsquo; intravenous insulin therapy, usually at a rate of 10 U / h d & rsquo; insulin or 0,1 U/kg/h, allows recovery of glucose metabolism and blocking ketogenesis.
  • compensation of potassium loss by & rsquo; addition of KCI in the infusion should be implemented immediately (1,5 at 2 g KCI / h) in the & rsquo; absence of electrocardiographic signs of & rsquo; hyperkalemia. It is then adjusted according to the results of monitoring of serum potassium and its evolution (controls after 2 and 4 hours). The presence of signs & rsquo; hypokalemia during the & rsquo; initial ECG can lead to differ 1 at 2 hours l & rsquo; introduction of the & rsquo; insulin.

Due to its increased risk of & rsquo; hypokalemia and early organ failure, the correction of & rsquo; acidosis by an infusion 500 ml of isotonic saline bicarbonate (14 g/L) n & rsquo; it is recommended that & rsquo; in case of & rsquo; severe acidosis (pH <7) persistent one hour after the start of treatment.

5- Surveillance :

  • arterial pressure, heart rate and breathing, diuresis, capillary blood glucose, Ketone Ketone or every hour during the 6 early hours ;
  • control of the & rsquo; ECG, s & rsquo; electrolytes, creatinine and blood gas 2 hours in the 4 or 6 early hours of treatment, then depending on the situation.

6- Complications :

– infectious (pneumonia, UTIs, oesophagites etc.) favored by dehydration, leading to limit the urinary catheter to comatose patients ; thromboemboliques ; digestive : hemorrhagic vomiting, acute pancreatitis ;
– iatrogènes :
– hypoglycemia,
– hypokalaemia
– severe hypophosphatemia with neurological symptoms and muscle and sometimes hemolytic anemia,
– brain edema by lowering too fast for the & rsquo; osmolarity,
– fluid overload with acute pulmonary edema
– hyperchloraemic acidosis favored by infusions of NaCl and KCl, usually without clinical consequences and resolved spontaneously.

C- hyperosmolar States :

C & rsquo; is severe hyperglycaemia without ketosis, accompanied by & rsquo; a major dehydration.

1- pathophysiology :

L & rsquo; s hyperosmolar state & rsquo; usually settles over several days in favor & rsquo; insulin deficiency, shallower than that leading to the & rsquo; & rsquo acidocétose.L; activation of hormone-regulating against leads to the progressive development of & rsquo; hyperglycemia, ketogenesis but remains moderate. L & rsquo; hyperglycemia triggers an osmotic polyuria and movement d & rsquo; intracellular water sector to the extracellular. Initially, polyuria s & rsquo; accompanied sodées losses, but as dehydration progresses, s & rsquo; installs a functional renal failure that will lead to a significant increase in the & rsquo; hyperglycemia and the & rsquo; & rsquo installation; hypernatremia.

2- Contributing factors :

The states hyperosmolar s & rsquo; settle in & rsquo; vast majority of cases in type diabetes 2 not using insulin. L & rsquo; age over 70 years, cognitive disorders, les limitations to the & rsquo; accès aux boissons, institutional living, a diuretic or corticosteroid therapy are frequently found predisposing factors. Very often, intervene infectious triggers (pneumonia, sepsis), neurological (AVC, subdural hematoma), myocardial infarction or digestive pathology.

3- clinical manifestations :

dehydration s & rsquo; installs resulting solely asthenia and weight loss.

Gradually, disorders of consciousness s & rsquo; worsen installation & rsquo; stupor, and d & rsquo; a deep coma, sometimes with partial onset seizures or generalized. The loss of & rsquo; water usually exceed 5 L. The intracellular dehydration predominates but the extracellular compartment is also concerned (fold skin, low blood pressure). Cardiovascular collapse s can & rsquo; install, especially if antihypertensive treatment.

4- Biology :

– Blood glucose generally exceeds widely 6 g/L

– l & rsquo; plasma osmolality 350 mOsm/L.- The serum sodium often appears normal initially, but its value must be corrected for the & rsquo; hyperglycemia [paint it + 1,6 (glucose – 1)]. It s & rsquo; student beyond 150 mmol / L in most forms of stigma sévères.-d & rsquo; hemoconcentration : elevation of & rsquo; hematocrit, in serum protein and the & rsquo; urea. -Serum potassium is usually normal because the output of potassium cellular compartment compensate urinary losses.

– Renal failure appears as the extracellular dehydration s & rsquo; highlights. It n & rsquo; there is no d & rsquo; metabolic acidosis, -l & rsquo; elevated lactate and |3-OH moderate remaining butyrate.

5- Treatment :

The priority is the correction of the & rsquo; hypovolemia and prevention of & rsquo; kidney failure and collapse administer 1 The isotonic saline the First Time, then 1 at 2 L of normal saline over the 3 following hours. Filling a macromolecular solute should be infused in the event of collapse.

Filling the water deficit after the initial correction of the & rsquo; hypovolemia should avoid & rsquo; use of hypotonic solutions in order not to cause too rapid fall of the & rsquo; osmolarity can lead to & rsquo; cerebral edema. A total of 6 at 10 The liquid will thus be administered 24 hours, half in the 8 early hours.

Potassium losses should be compensated based on the results of serum potassium, it n & rsquo; there is no major risk of & rsquo; severe hypokalemia due to the & rsquo; & rsquo absence; acidosis.

L & rsquo; continuous intravenous insulin therapy should aim to achieve a gradual reduction in blood glucose to values ​​of & rsquo; order 3 g / L after 12 hours.

Bedsore prevention, Nosocomial infections and thromboembolic complications (preventive heparin) is fundamental in these elderly, highly dehydrated.

Clinical monitoring is on heart rate, blood pressure, the diuresis, l & rsquo; state of consciousness. Cardiac monitoring is necessary in case of electrolyte disturbances. Capillary blood glucose should be monitored every hour. L & rsquo; blood electrolytes should be checked every 4 hours.

6- hyperosmolar coma Prevention :

Inform the patient and his family :

early manifestations, even with mild diabetes :

  • intense thirst,
  • polyurie,
  • rapid weight loss,
  • fatigue ;
  • predisposing or triggering circumstances :
  • intercurrent illness, in particular infectious,
  • neurological accident,
  • diuretic or corticosteroids,
  • heat wave.
  • Report l & rsquo; existence of diabetes and treatment taken during medical consultations or in case of & rsquo; surgery.
  • To behave :
  • ensure proper hydration ;
  • intensify or urinary glucose monitoring ;
  • call a physician in the event of major disruption of blood sugar.

D- lactic acidosis :

Lactic acidosis can occur in a diabetic subject in the same circumstances as in non-diabetic, but this complication may also be induced by metformin.

1- pathophysiology :

Production & rsquo; lactic acid resulting from the transformation under the & rsquo; effect of lactate dehydrogenase, pyruvate produced by glycolysis. This reaction normally leads to & rsquo; & rsquo obtain; lactate report / pyruvate 10 and lactate concentration in the rest of the & rsquo; order 0,75 mmol/L. aerobically, pyruvate can be converted into acétylCo-A, and enter in the Krebs cycle and lactate can be converted back to pyruvate in the presence of NAD (nicotinamide adénine dinucléotide) oxidized and then suffer the same fate. In situation & rsquo; tissue anoxia, l & rsquo; equilibrium shifts in the direction of lactate which is the final metabolite of glycolysis. Production & rsquo; lactic acid may well exceed the opportunities & rsquo; use tissue and & rsquo; hepatic and renal elimination and metabolic acidosis can s & rsquo; install, to & rsquo; origin & rsquo; a vicious circle involving the decrease in cardiac output and tissue perfusion and & rsquo; functional inhibition of pyruvate- liver carboxylase.

Metformin increases lactate production as it inhibits the phosphoenol pyruvate- carboxykinase which allows & rsquo; entry of pyruvate into the path of gluconeogenesis. Lactic acidosis and likely to develop in patients treated with metformin or in favor of & rsquo; intoxication Product (renal failure), either to the & rsquo; & rsquo occasion, tissue ischemia, and this even in the presence of normal plasma concentrations of metformin.

2- Clinical manifestations and biological :

During the prodromal phase : asthenia, muscle cramps, abdominal and chest pain which should lead to interrupt metformin immediately.

When & rsquo; acidosis is installed : a state & rsquo; anxious agitation, and disorders of consciousness, breathing acidotic, tachycardia, a drop in blood pressure and oliguria explaining the & rsquo; usual absence of dehydration, hypothermia. Not treated, l & rsquo; progresses to cardiovascular collapse, l&rsquo;anurie, arrhythmias associated with the & rsquo; hyperkalemia.

– Confirmation of the diagnosis based on the detection of & rsquo; d & a biological table rsquo; severe metabolic acidosis, the presence of & rsquo; an anionic hole much greater than 12 mmol / L and an increase in the arterial lactate above 6 mmol / L with an increase in the ratio lactate / pyruvate. L & rsquo; elevation of ketone bodies is usual. Renal function is usually impaired. Glucose is itself variable.

3- Treatment :

L & rsquo; lactic acidosis consists requires care in intensive care . Apart from general measures, treatment is based primarily on the restoration of the & rsquo; hemodynamic and ventilatory and treatment of & rsquo; causal affection. The fight against collapse requires fluid replacement and good tissue oxygenation.

Dialysis is useful in case of & rsquo; renal failure and when & rsquo; there metformin accumulation (plasma assay) because it is readily dialyzable

4- Preventive treatment :

It is based primarily on respect for cons-indications and precautions of Metformin in case of temporary -interruption & rsquo; severe intercurrent disease, d & rsquo; surgery or d & rsquo; iodinated contrast injection, Regular monitoring of serum creatinine in patients treated long-term, especially older, and in the presence of treatments that d & rsquo; impact renal function.

Course Dr S. Bensalem – Faculty of Constantine