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    Dka CPG

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    Mercemarie

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    Dka CPG

    Uploaded by

    Mercemarie
    3 views35 pages

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    DKA CPG

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    Dka CPG

    Uploaded by

    Mercemarie

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    of 35

    DIABETIC

    KETOACIDOSIS
    Mercemarie F. Atian
    Level I
    BMC Family and Community Medicine
    Objectives

    ■ Present a case of diabetic ketoacidosis and discuss the latest available guidelines to
    aid in diagnosing and managing such cases
    ■ Provide an algorithm that can guide us in our approach to patients presenting with
    diabetic ketoacidosis in primary care and to know when to refer to specialists
    General Data Patient A.M.
    Age: 33 y.o.
    Sex: Female
    Status: Single
    Address: Tiwi, Albay
    Religion: Roman Catholic
    Housewife
    Lives with 3 children and husband
    Chief Complaint

    ■ Lethargy
    History of Present Illness

    1 day PTC Few hours PTC


    ■ Patient attended a relative’s birthday ■ Patient was noted to be arousable but
    party in Iriga groggy even while having a meal
    ■ Afterwards, she had sudden onset ■ A few hours after, she was noted to be
    generalized abdominal pain with obtunded and became unarousable,
    associated nausea and vomiting, hence was rushed to the ER
    postprandial..they assumed it was just
    indigestion
    ■ No fever, chills, change in stool ■ At the ER:
    consistency or body malaise noted. CBG Reading: Hi (>500mg/dL)
    ■ No consult done.
    Review of Systems

    Systemic No fever, (-) weight loss


    HEENT No blurring of vision, ear pain, otorrhea, colds, sore throat,
    dysphagia, odynophagia, neck mass, dysgeusia, dental carries

    Cardio (-) palpitations, (-) PND (-) bipedal edema, (-) syncope

    Pulmo No hemoptysis, night sweats, (+) tachypnea


    GUT No dysuria, frequency, urgency, nocturia, weak stream, intermittency,
    incomplete emptying, hematuria, flank pain, lithiuria

    MSK No gait disturbance, arthralgia, myalgia, swelling, erythema, motor


    weakness
    Hema No easy bruisability, epistaxis, pallor, gum bleeding
    Derma No rashes, dry skin, scaling, pruritus
    Endo No polyuria, polydipsia, polyphagia, constipation/diarrhea, heat/cold
    intolerance
    Neuro No tremors, diplopia, anosmia, syncope
    PAST MEDICAL HISTORY
    Known case of DMT1, Unknown Control, lost to ff up
    NO KNOWN ALLERGY TO FOOD AND MEDICATIONS
    NO HISTORY OF PREVIOUS HOSPITALIZATIONS
    NO HISTORY OF SURGERIES
    NO HISTORY OF TRAUMA
    FAMILY HISTORY

    (+) HYPERTENSION, (+) DIABETES


    Maternal MELLITUS, Paternal

    (-) CANCER (-) PTB


    Housewife
    G3P3 (3003)
    LMP: 03/30/2024

    (-) Alcoholic beverage drinking


    Personal/Social (-) Cigarette Smoking
    (-) Betel Nut Chewing
    History

    Preference for salty and oily


    food
    PHYSICAL EXAMINATION
    General Survey Lethargic, GCS11 (E3V2M5)

    100/80, 114bpm. 31cpm, 37.2C, 95% RA


    Vital Signs
    WT: 42 kg, Ht: 152cm, BMI: 25kg/m2 (UW)
    Anicteric sclerae, pale palpebral conjunctivae, (+) sunken eyeballs
    HEENT (-) cervical lymphadenopathies, (-) tonsillopharnyngeal congestions
    (+) dry oral mucosa
    Chest and Lungs Equal chest expansion, (-) wheezes, (-) crackles

    Adynamic precordium, normal rate and regular rhythm, distinct S1 and


    Cardiovascular
    S2, no murmurs, (-) Jugular vein distention
    Flabby abdomen, normoactive bowel sounds, soft, nontender, no
    Abdomen
    tenderness, no masses
    Genito-urinary E/N

    Thready pulses on all extremities, capillary refill time > 2 secs,


    Extremities
    (-) edema/cyanosis, (+) poor skin turgor
    Salient Features

    ■ Shortness of breath
    ■ Lethargy
    ■ Decrease in sensorium
    ■ CBG reading: Hi
    ■ PMHx: DMT1, lost to follow up
    ■ (+) Family history DMT2
    ■ Underweight/Malnourished
    ■ Signs of moderate dehydration
    Primary Working Impression

    ■ T/C Diabetic Ketoacidosis


    ■ T/C Hypovolemic Shock
    ■ Diabetes Mellitus Type 1, Uncontrolled
    Differential Diagnoses

    ■ Hyperosmolar Hyperglycemic State


    ■ Sepsis
    ■ CNSI
    Unfortunately…

    ■ Relatives were advised that patient was ideally for close ICU monitoring and the
    relatives requested transfer to BRTTH since it’s closer to home…
    ■ Before transfer
    – IV fluids were initiated: PNSS 0.9 1L x 1h, then reevaluate after 1h
    – Administer Regular Insulin IV Bolus (0.1/kg) 4.2u stat and a continuous IV
    Infusion of regular insulin 4.2u/hr; then recheck CBG
    DIABETIC
    KETOACIDOSIS
    ■ Diabetic ketoacidosis is characterized by
    – a serum glucose level greater than 250 mg per dL
    – a pH less than 7.3
    – a serum bicarbonate level less than 18 mEq per L
    – an elevated serum ketone level, and dehydration
    ■ Insulin deficiency is the main precipitating factor
    Symptoms

    ■ polyuria with polydipsia (98 percent),


    ■ weight loss (81 percent)
    ■ fatigue (62 percent)
    ■ dyspnea (57 percent)
    ■ vomiting (46 percent)
    ■ preceding febrile illness (40 percent)
    ■ abdominal pain (32 percent)
    ■ polyphagia (23 percent)
    TREATMENT
    Fluid Replacement

    ■ saline 0.9% is started at 15 to 20 mL per kg per hour, or 1 L per hour initially


    ■ As the patient stabilizes, fluids can be lowered to 4 to 14 mL per kg per hour, or
    250 to 500 mL per hour.
    ■ Once the corrected sodium concentration is normal or high (greater than 135
    mEq per L [135 mmol per L]), the solution can be changed to saline 0.45%.
    ■ Dextrose is added when the glucose level decreases to 200 mg per dL (11.10
    mmol per L)
    Insulin

    ■ To further correct hyperglycemia, insulin should be added to intravenous fluids one to two
    hours after fluids are initiated
    ■ initial bolus of 0.1 units per kg should be given with an infusion of 0.1 units per kg per hour.
    ■ An infusion of 0.14 units per kg per hour is recommended in the absence of a bolus.
    ■ GOAL: Glucose level should decrease by about 50 to 70 mg per dL (2.77 to 3.89 mmol per L)
    per hour
    ■ Once the glucose level decreases to 200 mg per dL, the insulin infusion rate should be
    decreased to 0.05 to 0.1 units per kg per hour, and dextrose should be added to the
    intravenous fluids to maintain a glucose level between 150 and 200 mg per dL (8.32 and 11.10
    mmol per L)
    ■ Subcutaneous insulin is an effective alternative to intravenous insulin in persons with
    uncomplicated DKA
    DKA Resolved

    ■ Glucose level is less than 200 mg per dL


    ■ pH is greater than 7.3
    ■ Bicarbonate level is 18 mEq per L or higher
    ■ Insulin Regimen: Intermediate- or long-acting and short- or rapid-acting insulin
    ■ Known with diabetes: start outpatient dose, adjusted accordingly
    ■ Unknown/New: 0.5 to 0.8 per kg per day in divided doses
    Potassium

    ■ Potassium levels should be monitored every two to four hours in the early
    stages of DKA
    – Hydration alone will cause potassium to drop because of dilution.
    – Improved renal perfusion will increase excretion.
    – Insulin therapy and correction of acidosis will cause cellular uptake of
    potassium
    ■ If the potassium level is in the normal range, replacement can start at 10 to 15
    mEq potassium per hour
    ■ GOAL: maintain serum potassium levels between 4 and 5 mEq per L (4 and 5
    mmol per L
    Bicarbonate

    ■ Current American Diabetes Association guidelines continue to recommend


    bicarbonate replacement in persons with a pH lower than 6.9 using 100 mEq of
    sodium bicarbonate in 400 mL of sterile water with 20 mEq of potassium
    chloride at a rate of 200 mL per hour for two hours. This should be repeated
    every two hours until the patient’s pH is 6.9 or greater
    Phosphate and Magnesium

    ■ phosphate deficiency is linked with muscle fatigue, rhabdomyolysis, hemolysis,


    respiratory failure, and cardiac arrhythmia, replacement is recommended when the
    phosphate level falls below 1.0 mg per dL (0.32 mmol per L) or when these
    complications occur
    – Persons with anemia or respiratory problems and congestive heart failure may
    benefit from phosphate.
    – This can be achieved by adding 20 to 30 mEq of potassium phosphate to the
    intravenous fluid
    ■ Drop in magnesium, which can result in paresthesia, tremor, muscle spasm,
    seizures, and cardiac arrhythmia
    – It should be replaced if it falls below 1.2 mg per dL or if symptoms of
    hypomagnesemia develop
    COMPLICATIONS

    ■ Cerebral edema is the most severe complication of DKA.


    – occurs in 0.5 to 1 percent of all DKA cases and carries a mortality rate of 21
    to 24 percent. Survivors are at risk of residual neurologic problems
    – Risk factors:
    ■ younger age, new-onset diabetes, longer duration of symptoms, lower partial
    pressure of carbon dioxide, severe acidosis, low initial bicarbonate level, low
    sodium level, high glucose level at presentation, rapid hydration, and retained
    fluid in the stomach
    – Signs require immediate evaluation:
    ■ headache, persistent vomiting, hypertension, bradycardia, and lethargy and other
    neurologic changes
    ■ Others: hypokalemia, hypoglycemia, acute renal failure, and shock
    PREVENTION
    References

    ■ Kitabchi AE, Umpierrez GE, Murphy MB, et al.; American Diabetes Association.
    Hyperglycemic crises in diabetes. Diabetes Care. 2004;27(suppl 1):S98.
    Copyright 2009 American Diabetes Association.
    THANK YOU!

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