DKA and HHS
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Transcript of DKA and HHS
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Diabetic KetoacidosisHyperglycemic Hyperosmolar
State
Dr. Soumar DuttaPG Trainee
Accident and Critical Care Medicine
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Diabetic KetoacidosisDiabetic Ketoacidosis
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IntroductionIntroduction
ā¢ Acute life threatening complication of DM
ā¢ DKA predominantly seen in type 1 DM
ā¢ DKA represents bodyās response to cellular starvation due to insulin deficiency & counter regulatory hormone excess
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DKADKA
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ClassificationClassification
Mild DKA Moderate DKA Severe DKA
Plasma glucose > 250 mg/dl > 250 mg/dl > 250 mg/dl
Arterial ph 7.25-7.30 7.0-7.24 < 7.0
Serum bicarbonate 15-18 10-<15 < 10
Urine ketones + + +Anion gap >10 >12 >12
Alteration in sensorium alert alert/drowsy stupor/coma
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Pathophysiology of DKA Pathophysiology of DKA
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ā¢ Facilitate uptake of glucose & conversion into glycogenā¢ Inhibits glycogenolysis & gluconeogenesis
ā¢ Increase lipogenesisā¢ Inhibit lipolysis
ā¢ Uptake of amino acids into muscle cellā¢ Prevents release of amino acids from muscle
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PathophysiologyInsulin Deficiency is the primary defect in patients with DKA
Muscle Hepatocyte Adipose
Glucose
AminoAcids
Glucose-P
Glycogen
Pyruvate, CO2
Glucose
FreefattyacidsKetoacids
Normal Insulin Activity
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Pathophysiology
Insulin
GlucagonEpinephrine
CortisolGrowth Hormone
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Pathophysiology
Decreased Glucose UtilizationLipolysis
Insulin
GlucagonEpinephrine
CortisolGrowth Hormone
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DKA - EarlyDKA - Early
ā¢ Relative Insulin Deficiencyā¢ Glycogenolysis & gluconeogenesisā¢ Peripheral glucose uptake
Elevates blood glucose
Decreased Utilization post-prandial
and Stress-Induced
hyperglycemia
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Pathophysiology
GluconeogenesisGlycogenolysis
LipolysisKetogenesis
InsulinGlucagon
EpinephrineCortisol
Growth Hormone
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ā¢ Insulin Deficiency
GlycogenolysisGluconeogenesisHepatic glucose outputLipolysis: Release FFA -> liver VLDL & ketones Ketonemia and hyper TG
Acidosis , Hyperglycemia & Osmotic diuresis
DKA - LateDKA - Late Increased Production &Decreased Utilization Fasting hyperglycemia
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Islets of Langerhans
-cell destruction Insulin Deficiency
Adipo-cytes
Muscle
Liver
Decreased Glucose Utilization &Increased Production
GlucagonIncreasedProtein
CatabolismIncreasedKetogenesisGlucoaneogenesis,Glycogenolysis
IncreasedLipolysis
HyperglycemiaKetoacidosis
HyperTG
PolyuriaVolume Depletion
Ketonuria
AminoAcids
FattyAcids
StressEpi,Cortisol
GH,Glucagon
Threshold180 mg/dl
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Precipitating factors of DKAPrecipitating factors of DKA
ā¢ Omission or reduced daily insulin injectionā¢ Infectionā¢ Pancreatitisā¢ Myocardial Infarctionā¢ Mesentric Ischemiaā¢ Renal Insufficeincyā¢ CVA
ā¢ Pulmonary embolismā¢ G I hemorrhageā¢ Heat related illnessā¢ Parenteral/enteral
alimentationā¢ Rhabdomyolysisā¢ Severe Burns
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Drugs Precipitate DKADrugs Precipitate DKA
ā¢ Diureticsā¢ Lithiumā¢ Beta Blockersā¢ Mannitolā¢ Chlorpromazineā¢ Cimetidine
ā¢ Glucocorticoidsā¢ Neurolepticsā¢ Phenytoinā¢ Didanosineā¢ Calcium-channel
blockersā¢ Pentamidine
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Clinical featuresClinical features
Hyperglycemia
Osmotic diuresis and renal loss of Na, K, PO4, Ca and Mg
Hypovolemia,acidosis and hyperventilation
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Clinical featuresClinical features
ā¢ Increased PGI2 and PGE2peripheral vasodilation ,nausea, vomiting and abdominal pain.
ā¢ Vomiting maladaptive response to counter acidosis exacerbates the potassium losses
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Signs of DKASigns of DKA
ā¢ Dehydrationā¢ Hyperventilationā¢ Ketotic breathā¢ Tachycardia and hypotensionā¢ Disturbed conscious state and shock
ā¢ Alteration of consciousness correlate better with elevated serum osmolality (>320 mOsm/L) than with severity of metabolic acidosis
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SymptomsSymptoms
ā¢ Polyuria
ā¢ Polydipsia
ā¢ Nausea and vomiting
ā¢ Abdominal Pain
ā¢ Breathing difficulty
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Lab InvestigationsLab Investigations
ā¢ Serum glucoseā¢ Serum electrolytesā¢ Complete blood countā¢ Renal function testā¢ Serum & urine ketonesā¢ Blood gas analysis
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Lab InvestigationsLab Investigations
ā¢ Blood culturesā¢ Sputum collection ā¢ Urine analysis & Cultureā¢ Liver function tests & Coagulation profiileā¢ Cardiac enzymesā¢ Thyroid function testsā¢ Toxicological Screening
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RadiologyRadiology
ā¢ Chest X ray
ā¢ ECG
ā¢ USG Abdomen
ā¢ CT Head
ā¢ Lumbar Puncture
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Corrected SodiumCorrected Sodium
Measured Na + 1.6 (Glucose-100)
100ā¢Na+ depressed 1.6 mEq/L per 100 mg% glucose rise above 100 mg/dl.
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Corrected SodiumCorrected Sodium
Example:Na+ = 123 meq/L and Glucose = 1,250 mg/dl
Measured Na + 1.6 (Glucose-100) 100
= 123 + 1.6 (1250-100) 100Corrected Na+ = 123 + 18 = 141 meq/L
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Serum OsmolaritySerum Osmolarity
2(Na) + Glucose + BUN 18 2.8
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D/D
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Management of DKAManagement of DKA
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Goals of TreatmentGoals of Treatment
ā¢ Volume Repletionā¢ Reversal of metabolic consequences of
insulin insufficiencyā¢ Correction of acid-base & electrolyte
imbalancesā¢ Recognition & Treatment of precipitating
causesā¢ Avoidance of complications
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Management of DKAManagement of DKA
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Approach to therapyApproach to therapy
ā¢ Correcting the hyperosmolar state and dehydration is the initial aim of therapy.
ā¢ Insulin therapy should be undertaken only after the patient is stable hemodynamically.
Glucose and H2O
H2O lost in urine Loss of ECF, vascular collapse and death
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Fluid ResuscitationFluid Resuscitation
ā¢ Single most important stepā¢ Fluid deficit around 100ml/kg (5-10L)ā¢ Helps in Restore I/V volumeā¢ Perfuse vital organsā¢ Increase GFRā¢ Decrease serum Glucose & Ketone levelsā¢ To restore normal tonicity
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Fluid balance in diabeticFluid balance in diabetichyperosmolarityhyperosmolarity
ECF = 14 L ICF = 28 L
H2O
ECF ICF
H2O
Osmotic Diuresis
Osmotic Diuresis ECF hyperosmolar from ICF autotransfusion
ECF and ICF both hyperosmolar
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Fluid ResuscitationFluid Resuscitation
ā¢ NS most frequently administered fluidā¢ 1 litre in 30 minā¢ 2 litres in 2 hoursā¢ 2 litres in 2-6 hoursā¢ 2 litres in 6-12 hours
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Fluid ResuscitationFluid Resuscitation
ā¢ 2ā3 L of 0.9% saline over first 1ā3 h (10ā15 mL/kg per hour)
ā¢ 0.45% saline at 150ā300 mL/h; change to 5% glucose and 0.45% saline at 100ā200 mL/h when plasma glucose reaches 250 mg/dl.
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Fluid ResuscitationFluid Resuscitation
ā¢CVP guided fluids should be considered for elderly & those with heart disease
ā¢Excess fluid may lead to ARDS & cerebral edema
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Insulin therapyInsulin therapy
Mechanism of Action:
ā¢ Inhibit gluconeogenesis, lipolysis, catabolic
hormone secretion, production of ketoacids
ā¢ Promote potassium, glucose & phosphate
uptake in tissues
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Insulin therapyInsulin therapy
ā¢ Ideal way to administer insulin by continuous infusion of small doses of regular insulin 0.1unit/kg/hr once hypokalemia is excluded.
ā¢ I/M or S/C administration of regular insulin should be avoided as insulin absorption may be erratic in volume depleted & vasocostricted patient
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Insulin therapyInsulin therapy
ā¢ Goal is to decrease Glucose by 50-75mg/dl/hr.50-75mg/dl/hr.
ā¢ Infusion should continue until anion gap normalized
ā¢ S/C insulin should bridge for atleast one hour before discontinuation of I/V insulin
ā¢ Insulin administration should be W/H if K <3.3 mEq till K is supplemented
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DKA: Switch to S.C. insulinDKA: Switch to S.C. insulin
Can consider switch to SC insulin when:
ā¢ AG normalizedā¢ BS < 250 mg/dlā¢ Insulin IV requirements < 2U/hā¢ Patient able to eatā¢ Hemodynamically stable
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DKA: Switch to S.C. insulinDKA: Switch to S.C. insulin
ā¢ Overlap insulin IV with 1st SC insulin by 2-4h to avoid recurrent ketosis
ā¢ T2 DM patients with DKA:ā¢ Donāt necessarily have to be continued on
insulinā¢ Once acute stress resolved, many do well on
OHA
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Potassium CorrectionPotassium Correctionā¢ K+ defecit: 3-5 mEq/Kg (350 mEq for 70Kg)ā¢ Normal to high serum K+
K+ K+H+ H+
Ketoacidosis
Insulin
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Potassium CorrectionPotassium Correction
ā¢ Deficiency is due to
ā¢ Decreased insulin levelsā¢ Metabolic Acidosisā¢ Osmotic Diuresisā¢ Frequent Vomitting
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Goal of K ReplacementGoal of K Replacement
ā¢ To maintain a normal extracellular K+ conc during
the acute phase of therapy and to replace intra-
cellular deficits over a period of days
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K SupplementationK Supplementation
Serum Potassium < 3 mEq/L Give 60mEq/l to IVF
3-3.9 mEq/L 40mEq/l to IVF
4-5.4 mEq/L 20 mEq/L to IVF
> 5.5 mEq/L No Replacement necessary
Verify Normal kidney function & Urine output before treatment
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BicarbonateBicarbonate
ā¢ Routine use of supplemental bicarbonate in
Rx of DKA is not recommended
ā¢ Can be given if PH Is less than 6.9
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ADA RecommendationADA Recommendation
If PH 6.9-7.0 50mEq of NaHCo3+200ml sterile water+10mEq KCl over 1 hour
If Ph <6.9 100mEq of NaHCo3+400ml sterile water+10mEq KCl over 2 hours
Repeat dose of bicarb every 2 hours till PH>7
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Theoretical AdvantagesTheoretical Advantages
ā¢ In case of severe acidosis
ā¢ Improve myocardial contractility
ā¢ Improve catecholamine tissue response
ā¢ Decrease work of breathing
ā¢ In case of Hyperkalemia
ā¢ Elevate ventricular fibrillation threshold
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DisadvantagesDisadvantages
ā¢ Severe & worsening hypokalaemia
ā¢ Paradoxical CNS acidosis
ā¢ Impair oxyhemoglobin dissociation
ā¢ Hypertonicity
ā¢ Sodium overload
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DisadvantagesDisadvantages
ā¢ Delayed recovery from ketosis
ā¢ Elevation of lactic levels
ā¢ Precipitation of cerebral edema / Pulmonary
edema
ā¢ Thrombophlebitis
ā¢ Require Central venous cannulation
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HypophosphatemiaHypophosphatemia
ā¢ Most severe 24-48 hours after treatmentā¢ Treatment If Levels <1.0 mg/dlā¢ C/F
ā¢ Hypoxiaā¢ Rhabdomyolysisā¢ Hemolysisā¢ Respiratory failureā¢ Cardiac Dysfunction
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HypophosphatemiaHypophosphatemia
ā¢ IV (K2PO4 ) : 1ml/hr. (4.4 mEq potassium + 93 mg
phosphate )
ā¢ S/Eā¢ Hyperphosphatemiaā¢ Hypocalcemiaā¢ Hypomagnesemiaā¢ Metastatic soft tissue calcificationā¢ Hypernatremiaā¢ Osmotic diuresis
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HypomagnesemiaHypomagnesemia
ā¢ Inhibit parathyroid hormone secretionā¢ hypocalcaemia & hyper phosphatemia
ā¢ Supplementation if Mg <1.2 mg/dl
ā¢ Can give Oral Magnesium oxide orā¢ Parenteral Magnesium sulphate
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Monitoring Monitoring
ā¢ Periodical assessment of vital signs
ā¢ Level of consciousness
ā¢ Hourly urine output
ā¢ Serum glucose Q1H
ā¢ Serum Potassium Q2H
ā¢ Regular assessment of anion gap
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Complications of DKA Complications of DKA
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DKA in PediatricsDKA in Pediatrics
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Criteria for diagnosisCriteria for diagnosis
ā¢ Hyperglycemia: CBG > 300mg/dl.
ā¢ Metabolic acidosis:pH < 7.25 ā 7.30
HCO3- < 15 mEq/L
ā¢ Ketonemia
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Clinical featuresClinical features
ā¢ Polyuriaā¢ Polydipsiaā¢ Polyphagiaā¢ Abdominal painā¢ Nausea and vomitingā¢ Rapid weight lossā¢ Fatigue
ā¢ Confusionā¢ Visual changes
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SignsSigns
ā¢ Dehydrationā¢ Tachycardiaā¢ Hypotensionā¢ Kussmaul respiration (rapid & deep)ā¢ Sweet, fruity odour on the breath ā¢ LOC/Coma (look for cerebral edema)
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Treatment goalsTreatment goals
ā¢ Establish good perfusion statusā¢ Reverse the acidosisā¢ Correct electrolyte disturbancesā¢ Control hyperglycemia ā¢ Ketonemia
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TreatmentTreatment
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Correction of acidosisCorrection of acidosis
Donāt use bicarbonate asā¢ It will increase chances of cerebral edema
by 4 times.ā¢ can lead to volume overload,
hypernatremia, paradoxical cerebral acidosis, accelerated K+ loss
Is there any role for bicarbonate in DKA?
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Indication for bicarbonateIndication for bicarbonate
ā¢ pH < 7.0ā¢ Hemodynamically unstableā¢ Not responding to fluidsā¢ Depressed cardiac contractiltyā¢ Poor perfusion
Dose: 0.5 ā 2 mEq/kg over 1-2 hrs
Stop correction once pH >7.0
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Major complication of DKAMajor complication of DKA
ā¢ Cerebral Edema: most dreaded complicationā¢ 57-87% of all pediatric DKA-
associated deathsā¢ More in < 5yrs Rare in > 20 yrs.
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Reasons for Cerebral EdemaReasons for Cerebral Edema
ā¢ Over aggressive fluid correctionā¢ Failure of Na+ to rise with fall of glucose
during treatmentā¢ Cerebral ischemia due to severe dehydration
and hypocarbia
Onset : 6-12 hrs. after onset of therapy
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Clinical features Clinical features
ā¢ Severe headacheā¢ Seizuresā¢ Papilledemaā¢ Respiratory arrestā¢ Altered mental status
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Hyperglycemia Hyperosmolar State (HHS)
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IntroductionIntroduction
ā¢ A metabolic emergency that occurs in diabetic patient usually Type 2 Diabetes Mellitus
ā¢ Characterised by uncontrolled hyperglycemia that induces hyperosmolar state and dehydration without significant ketoacidosis.
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Diagnostic featuresDiagnostic features
ā¢ Plasma glucose level of 600 mg/dL or greater
ā¢ Effective serum osmolality of 320 mOsm/kg or greater
ā¢ Profound dehydration (8-12 L) with elevated serum urea nitrogen (BUN)-to-creatinine ratio
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Diagnostic featuresDiagnostic features
ā¢ Small ketonuria and absent-to-low ketonemia
ā¢ Bicarbonate concentration greater than 15 mEq/L
ā¢ Some alteration in consciousness
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DKA Vs. HHSDKA Vs. HHSDKA HHS
Glucose 250-600 >600
Sodium 125-135 135-145
Potassium Normal/inc Normal
Bicarbonate <15meq/l Normal/slightly reduced
Arterial pH <7.3 >7.3
Anion gap Increased Normal/slightly increased
pCO2 20-30 Normal
Osmolality 300-320 >320
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CausesCauses
ā¢ Dehydrationā¢ Pneumonia and UTIā¢ Counter-regulotary
hormone (e.g cortisol, cathecolamine, glucagon)
ā¢ Dialysisā¢ TPNā¢ Non-compliance to OHA
or insulin therapy
Drugsā¢ Diureticsā¢ B-blockerā¢ Histamine(H2)
Blockerā¢ Anti-psychotics
Clozapine, Olanzapine
ā¢ Alcohol and cocaine
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PathophysiologyPathophysiologyConcomitant illness
Circulating insulin& of counter-regulatory hormones
renal clearance and peripheral utilization of glucose
Hyperglycemia Osmotic diuresis
Loss of electrocyte and water
Dehydration
Hyperosmolarity Intracellular dehydration
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Clinical featuresā¢ Occurs only in type 2 DM
ā¢ Could be initial presentation of the diabetic state
ā¢ Elderly
ā¢ Obtundation to coma
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Clinical featuresā¢ Severe dehydration invariable
ā¢ May have associated lactic acidosis due to hypoxia
ā¢ Precipitating factors similar to DKA
ā¢ Mortality rate is high
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SymptomsSymptoms
Symptoms of hyperglycemia :PolydipsiaPolyuriaLethargic
Others :Weight lossLoss of consciousness
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SymptomsSymptoms
A wide variety of focal and global neurologic changes may be present :
ā¢ Drowsiness and lethargyā¢ Deliriumā¢ Comaā¢ Focal or generalized seizuresā¢ Visual changes or disturbancesā¢ Hemiparesisā¢ Sensory deficits
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Physical examination Physical examination
Dehydrated : dry skin, lips, mucous membrane, loss skin turgor
Vital sign : tachycardia (early dehydration), hypotension (later), temperature
Systemic examination to ruled out the cause.
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Differential diagnosisDifferential diagnosis
ā¢ Alcoholic ketoacidosisā¢ Delirium (altered mentation)ā¢ Dementiaā¢ Overdoseā¢ Thyrotoxicosis (tachycardia, fever,
dehydration)
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Lab studiesLab studiesā¢ Plasma glucose
Hyperglycemia: CBG : > 600 mg/dlā¢ ABG
PH> 7.3HCO3>15 mmol/l
ā¢ Serum osmolality>320 mmol/l
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OthersOthers
ā¢ Urine-analysisā¢ Exclude UTIā¢ Proteinuria
ā¢ Plasma ketoneā¢ Plasma electrolyteā¢ Renal function test( Creatinine &BUN)ā¢ CBCā¢ Creatine kinase
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Imaging studiesImaging studies
Chest radiographā¢ Exclude pnuemoniaā¢ Cardiomegaly
CT scan of the headā¢ Exclude haemorrhagic stroke, subdural
haematomaā¢ Look for cerebral edema
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ManagementManagement
Treatment Goals:
ā¢ Correction of hypovolemiaā¢ Identify and treating underlying causeā¢ Correcting electrolyte abnormalitiesā¢ Gradual correction of hyperglycemia and
osmolarityā¢ Frequent monitoring
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ManagementManagement
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References
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Thank You