Anaphylaxis and Diabetic coma....


Anaphylaxis

อาการและอาการแสดงตั้งแต่ 2 ระบบขึ้นไป

     –        Skin : flushing, urticaria, angioedema

     –        CV : tachycardia, hypotension, syncope, arrhythmia

     –        GI : nausea, vomiting, diarrhea, abdominal distension

     –        Respiratory : rhinorrhea, laryngeal edema, wheezing, asphyxia, pulmonary edema

     –        Neuro : loss of consciousness, headache, disorientation

Anaphylaxis (treatment)

ABC, iv, O2, monitor

Epinephrine

     –        0.3-0.5 ml (0.01ml/kg in children) of epinephrine 1:1000

     –        Maintain blood pressure

    –        Inhibit mediator release by Increasing intracellular cAMP

    –        bronchodilatation

Antihistamine ( 48 hours)

    –        H1 blocker : diphenhydramine, chlorpheniramine

    –        H2 blocker : cimetidine, ranitidine

Corticosteroid

Inhaled beta agonist

Vasopressor : for hypotension not response to iv fluid

    –        Dopamine

    –        Levophed

Status epilepticus

     Continuous seizure >= 30 mins

     >=2 seizures without full recovery of consciousness

     Morbidity : hypoxia, hyperthermia, circulatory collapse, neuronal injury

    Secondary cause

        Drug intoxication

        Eclampsia

        Intracranial pathology

       Metabolic: hypoglycemia, hyponatremia

       CNS infection

Status epilepticus (treatment)

     ABC, iv, O2, monitor

     DTX ( thiamine+glucose)

     Anticonvulsant

        –        Diazepam 5 mg iv every 5 mins, upto 20 mg

        –        Dilantin 20 mg/kg iv at 50 mg/min

       –        Additional dilantin 5-10 mg/kg iv

       –        Phenobarb 20 mg/kg iv, additional 5-10 mg/kg

      –        General anesthesia ( midazolam, propofal, thiopental)

    Supportive care

         –        Cooling, foley’s catheter

Diabetic coma

    Hyperglycemic crisis

          –        Diabetic ketoacidosis (DKA)

         –        Hyperosmolar hyperglycemic state (HHS) or        Hyperosmolar hyperglycemic nonketotic coma (HHNC)

     Hypoglycemic coma

Diabetic ketoacidosis (DKA)Pathogenesis

    Insulin deficiency

    Counterregulatory hormone excess   ( glucagon, cathecolamine, cortisol, growth hormone)

       –        Hyperglycemia

       –        High serum osmolarity

       –        Loss of water and electrolyte due to glucosuria ( osmotic diuresis)

       –        Ketosis and metabolic acidosis due to lipolysis, fatty acid oxidation, ketoacid formation

Diabetic ketoacidosis (DKA)Precipitating factor

     Error in insulin used

     Stress events

           –        Infection, stroke, MI, trauma, pregnancy, hyperthyroidism, pancreatitis, pulmonary embolism, surgery, steroid use

     25% no clear causes

Diabetic ketoacidosis (DKA) Clinical presentation

     Hyperglycemia : polyuria, polydipsia

     Volume depletion : tachycardia, hypotension

     Acidosis : kussmaul respiration

     Abdominal pain, vomiting

     Mental status change, coma

Diabetic ketoacidosis (DKA) Diagnosis

     Blood glucose > 250 mg/dl

     Acidosis :

          –        arterial pH <7.3

         –        serum bicarbonate <15

     Ketonuria and increased serum ketone

Diabetic ketoacidosis (DKA) Differential diagnosis

      High anion gap metabolic acidosis

         –        Methanol

         –        Uremia

        –        DKA/ AKA

        –        Paraldehyde

        –        Iron/ INH

        –        Lactic acid

       –        Ethylene glycol

       –        Salicylate

Diabetic ketoacidosis (DKA) Treatment

      Volume repletion

      Reversal of metabolic consequence

      Correct electrolyte and acid-base imbalance

      Treat precipitating causes

      Avoid complication

      Fluid

           0.9%NSS 1000-1500 ml in 1st hour

           500-1000 ml/hr in 2nd-3rd hour

           250 ml/hr in 4th-8th hour

          125 ml/hr later

      Insulin

      RI 10 U (0.15U/kg) iv bolus, then 0.1 U/kg/hr iv infusion

      Blood glucose should decrease 75-100 mg/dl/hr

      Patassium

            K initially may increased ( acidosis, hemoconcentration)

            K will decrease rapidly after treatment of DKA

            Every patients should get K supplement unless K >5.5

           Don’t give RI if K <3.5

      Bicarbonate

                If pH<7
หมายเลขบันทึก: 19323เขียนเมื่อ 16 มีนาคม 2006 16:52 น. ()แก้ไขเมื่อ 13 มิถุนายน 2012 21:34 น. ()สัญญาอนุญาต: จำนวนที่อ่านจำนวนที่อ่าน:


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