DKA & HHS

Ahmad F. Mady MD

04/18/23 04:04 PM

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Diabetes

1552 BC, Diabetes 1st Described In Writing on 3rd

Dynasty Eqyptian papyrus by physician Hesy-Ra:

mentions polyuria as a symptom.

250 BC, Apollonius of Memphis coined the name

"diabetes” meaning "to go through" or siphon. He

understood that the disease drained more fluid than a

person could consume.

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Diabetes Mellitus

Gradually the Latin word for honey, "mellitus," was added to

diabetes because it made the urine sweet.

Up to 11th century diabetes was commonly diagnosed by

“water tasters” who drank the urine of those suspected of

having diabetes, as it was sweet-tasting.

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Early Diabetes Discoveries

In the 1869, Paul Langerhans, a German medical student

announced in a thesis, that the pancreas contains two systems

of cells.

In the1889 Oskar Minkowski and Joseph von Mering in France,

removed the pancreas from a dog to determine the effect of an

absent pancreas on digestion

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Fredrick Banting & Charles Best

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Leonard Thompson

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Three months later

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Ppt Factors of DKA&HHS

FactorApproximate frequency

Infection35%

Omission of insulin or inadequate insulin

30%

Initial presentation of

diabetes mellitus

20%

Medical illness10%

Unknown5%

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Clinical Presentation of DKA

History of polyuria, polydipsia, polyphagia, weight loss Nausea, vomiting, abdominal pain Acidemia leading to hyperventilation,Kussmaul

breathing,Ketotic odour. Clouding of sensorium, weakness, and coma Dehydration and shock

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Clinical Presentation of HHS

Similar to DKA but coma is more frequent Severe dehydration is the rule Focal neurologic deficits may be found at

presentation Usually more elderly patients Acidemia not pronounced

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Laboratory Findings

Serum osmolality290+_10<320>320

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Treatment involves 5 key components:

Monitoring Fluid resuscitation Insulin and dextrose infusion Electrolyte repletion Treating underlying cause

Therapeutic goals

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Dehydration

WHY?……

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Fluids, fluids, fluids!

Restores circulatory volumeDiminish concentration of catecholamines, glucagon

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Caution!

Excessive therapy may result in ARDSCerebral edemaHyperchloremic acidosis

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Fluid replacement in DKA

Initial fluid = normal saline– 15ml to 20ml/kg, about 1-2L in 1 hour– 500 ml/h for next 2 hours or 1L /h if in shock– 500-250 ml/h according to hydration status (RBS 250mg/dl)

Subsequent change in fluids– half normal saline

START when urine output improves and BP stable– D5 1/2 NS

START when blood glucose <250 mg/dl Endpoint

- resolution of ketonemia and acidosis

- Se bicarbonate >18

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If SBP<90 mmHg

Initially give 1 litre of Normal Saline per hour.

If SBP>90 mmHg

0.45% N/S if serum sodium is high or normal

0.9% N/S if serum sodium is low.

Rate and volume as for DKA.

Rate should be adjusted for cardiac function

Fluid replacement in HHS

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Insulin administration in DKA&HHS

Withhold insulin therapy until the serum potassium

concentration has been determined.

Initial regular insulin

– Goal = reduce hourly glucose by 50-70 mg/dl

– Bolus = 0.15u/kg or 10u bolus

– IV infusion = 0.1u/kg/hr till RBS 250mg/dl then follow iv

infusion protocol

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Insulin administration in DKA&HHS

Endpoint for continuous/hourly regular insulin– Se bicarbonate >18, anion gap <14– Absence of serum ketones

Switch over to maintenance

Plasma glucose is less than 250 mg/dl

DKA has resolved

Patient is tolerating PO

It is important to give the first s.c. injection of insulin approximately 2 hours before stopping the i.v. route

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Intravenous Insulin Infusion Protocol

Capillary blood glucose in mg/dl (mmol/L)

Units of Insulin per Hour

<99 (5.5)0.5

100-149 (5.6-8.2)1

150-199 (8.3-11.0)2

200-249 (11.1-13.8)3

250-299 (13.9-16.6)4

300-349 (16.7-19.4)5

350-399 (19.5- 22.2)6

400-450 (22.3-24.9)8

>450 (24.9)10

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Who saved me: the insulin or the nurse ?

Who saved me: the insulin or the nurse ?

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Potassium Therapy

may be normal or elevated at the time of diagnosis

Goal is to maintain Se K between 4 and 5

If serum K>5 do not give K but recheck in one hour If serum K is 4-5 give KCl 20 mEq in each litre of fluid If serum K is 3-4 give KCl 30 mEq in each litre of fluid If serum K is <3 hold insuline,give KCl 40 mEq over 1hr then

recheck K

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Bicarbonate Therapy

Controversial– Most literature shows no benefit to using bicarbonate with

patients who have DKAor HHS No differences in reduction of glucose or ketoanion May increase hypokalemia, cerebral acidosis and

cardiac dysfunction– For patients with pH < 7.0, they may benefit from

bicarbonate therapy pH 6.9-7.0 may give 50 mEq of bicarb pH <6.9, may give 100 mEq of bicarb

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Phosphate Therapy

Phosphate deficiency– Osmotic diuresis → urinary phosphate losses– Insulin therapy → serum phosphate reenters intracellular compartment

Adverse complications may occur if P < 1.0 mg/dl

– Respiratory depression– Skeletal muscle weakness– Hemolytic anema– Cardiac dysfunction

May be useful to replace 1/3 potassium as K3PO4,reduce chloride load, prevent hyperchloremic acidosis.

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Investigations to be done

Serum glucose initially then hourly Serum K initially then hourly if <3 or >5 otherwise 2 hourly till stable Na, urea, creatinine initially then 4 hourly till stable ABG initially then as often as necessary Serum osmolality & Na hourly initially in HHS CBC with differential white count ECG, CXR Urine analysis Urine culture if pus cells or bacteria in U/A or patient is septic Blood culture if patient is febrile or WBC>12,000 Serum Mg and Ca Cardiac enzymes if ECG abnormal initially and after 8 hours Throat swab culture if signs of pharyngitis present Sputum culture if purulent looking or infiltrate on CXR Serum amylase (often raised-up to 10 times-even in the absence of pancreatitis)

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Avoid overhydration Note: Nitroprusside can be used to detect ketones but is not

accurate ….why? Prophylaxis small doses of LMW heparin Antibiotics: NOT routine Do consider anti-peptic ulcer prophylaxis

Considerations in management

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Complications

Lactic acidosis– Due to prolonged dehydration, shock, infection and tissue hypoxia

– Should be suspected in pt with refractory metabolic acidosis and

persistent anion gap Arterial thrombosis

– Stroke, MI, or an ischemic limb Cerebral edema

– Over hydration of free water, excessively rapid correction of

hyperglycemia are risk factors ARDS

– Excessive crystalloid infusion

– Pulmonary rales, increased AaO2 gradient

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Mortality from DKA

is due to?

1) Hyperglycemia

2) Acidosis

3) Sepsis

4) Hypokalemia

5) Cerebral edema

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Protocol

DKA

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Three Take Home Messages

1. DKA &HHS may be life threatening

2. Fluids and Insulin along with frequent

monitoring is essential

3. Watch for hypokalemia and cerebral edema

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Thank you for your attention

Thank you for saving me from DKA&HHS

Thank you for saving me from DKA&HHS

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Thank youThank you

AAHHMMAADD FF. . MMAADDYY MD MD