Acute Complications of DM

7/28/2019 Acute Complications of DM

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Prof. Iftikhar Ali Shah


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Acute Complications of Diabetes

DKA

HHNK

Hypoglycemia

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Other Complications Hypoglycemic Unawareness

Somogyi Phenomenon

Dawn Phenomenon

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Some things to know Dawn Phenomenon vs Somogis effect

Dawn phenomenon Blood sugar rises in early morning

Somogis (rebound) effect

Blood sugar rise in morning as reaction to hypoglycemic timeduring the night


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Chronic Complications Macrovascular Complications

Microvascular Complications

Neuropathic Complications

Mixed

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Diabetic Ketoacidosis


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Introduction DKA is an acute life threatening complication of DM

of hospital admissions for DM

Occurs predominantly in type I though may occur in II

Incidence of DKA in diabetics 15 per 1000 patients

20-30% of cases occur in new-onset diabetes

Mortality less than 5%

Mortality higher in elderly due to underlying renal disease or coexistinginfection

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Definition Exact definition is variable

Most consistent is: Blood glucose level greater than 250 mg/dL

Bicarbonate less than 15 mEq/L

Arterial pH less than 7.3

Moderate ketonemia

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Pathophysiology Bodys response to cellular starvation

Brought on by relative insulin deficiency and counter regulatory or catabolichormone excess

Insulin is responsible for metabolism and storage of carbohydrates, fat and protein

Lack of insulin and excess counter regulatory hormones (glucagon,catecholamines, cortisol and growth hormone) results in: Hyperglycemia (due to excess production and underutilization of glucose) Osmotic diuresis Prerenal azotemia Ketone formation

Wide anion-gap metabolic acidosis

Clinical manifestations related to hyperglycemia, volume depletion andacidosis

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Pathophysiology Free fatty acids released in the periphery are bound to albumin

and transported to the liver where they undergo conversion toketone bodies The metabolic acidosis in DKA is due to -hydroxybutyric acid and

acetoacetic acid which are in equilibrium Acetoacetic acid is metabolized to acetone, another major ketone body

Depletion of baseline hepatic glycogen stores tends to favor ketogenesis

Low insulin levels decrease the ability of the brain and cardiac andskeletal muscle to use ketones as an energy source, also increasingketonemia

Persistently elevated serum glucose levels eventually causes an osmoticdiuresis

Resulting volume depletion worsens hyperglycemia and ketonemia

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Electrolytes

Renal potassium losses already occurring from osmotic diuresis worsen due to renin-angiotensin-aldosterone system activation by volume depletion

In the kidney, chloride is retained in exchange for the ketoanions being excreted

Loss of ketoanions represents a loss of potential bicarbonate

In face of marked ketonuria, a superimposed hyperchloremic acidosis is also present

Presence of concurrent hyperchloremic metabolic acidosis can be detected by noting abicarbonate level lower than explainable by the amount the anion gap has increased

As adipose tissue is broken down, prostaglandins PGI2 and PGE2 are produced This accounts for the paradoxical vasodilation that occurs despite the profound levels of

volume depletion

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DKA in Pregnancy Physiologic changes in pregnancy makes more prone toDKA

Maternal fasting serum glucose levels are normally lower

Leads to relative insulin deficiency and an increase in baseline free fattyacid levels in the blood

Pregnant patients normally have increased levels of counterregulatory hormones

Chronic respiratory alkalosis Seen in pregnancy

Leads to decreased bicarbonate levels due to a compensatory renalresponse

Results in a decrease in buffering capacity

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DKA in Pregnancy Pregnant patients have increased incidence of vomitingand infections which may precipitate DKA

Maternal acidosis: Causes fetal acidosis

Decreases uterine blood flow and fetal oxygenation

Shifts the oxygen-hemoglobin dissociation curve to the right

Maternal shifts can lead to fetal dysrhythmia and death

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Causes of DKA 25% have no precipitating causes found

Errors in insulin use, especially in younger population

Omission of daily insulin injections

Stressful events: Infection Stroke MI Trauma

Pregnancy Hyperthyroidism Pancreatitis Pulmonary embolism Surgery Steroid use

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Clinical Features Hyperglycemia

Increased osmotic load

Movement of intracellular water into the vascular compartment Ensuing osmotic diuresis gradually leads to volume loss and renal

loss of sodium, chloride, potassium, phosphorus, calcium andmagnesium

Patients initially compensate by increasing their fluidintake

Initially polyuria and polydipsia are only symptoms untilketonemia and acidosis develop

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Clinical Features As acidosis progresses

Patient develops a compensatory augmented ventilatory response

Increased ventilation is stimulated physiologically by acidemia to

diminish PCO2 and counter the metabolic acidosis

Peripheral vasodilation develops from prostaglandins andacidosis Prostaglandins may contribute to unexplained nausea, vomiting

and abdominal pain Vomiting exacerbates the potassium losses and contributes to

volume depletion, weakness and weight loss

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Clinical Features Mental confusion or coma may occur with serumosmolarity greater than 340 mosm/L

Abnormal vital signs may be the only significantfinding at presentation

Tachycardia with orthostasis or hypotension areusually present

Poor skin turgor

Kussmaul respirations with severe acidemia17


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Clinical Features Acetone presents with odor in some patients

Absence of fever does not exclude infection as asource of the ketoacidosis

Hypothermia may occur due to peripheralvasodilatation

Abdominal pain and tenderness may occur withgastric distension, ileus or pancreatitis Abdominal pain and elevated amylase in those with

DKA or pancreatitis may make differentiation difficult Lipase is more specific to pancreatitis 18


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Clinical Suspicion If suspect DKA, want immediately:

Acucheck

Urine dip

ECG

Venous blood gas

Normal Saline IV drip

Almost all patients with DKA have glucose greaterthan 300 mg/dL

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Acidosis Elevated serum -hydroxybutyrate and acetoacetate causeacidosis and ketonuria

Elevated serum ketones may lead to a wide-anion gap metabolic

acidosis

Metabolic acidosis may occur due to vomiting, osmotic diuresisand concomitant diuretic use

Some with DKA may present with normal bicarbonateconcentration or alkalemia if other alkalotic processes are severeenough to mask acidosis In which case the elevated anion gap may be the only clue to the presence

of an underlying metabolic acidosis

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ABGs

Help determine precise acid-base status in order todirect treatmentVenous pH is just as helpful Studies have shown strong correlation between arterial and

venous pH in patients with DKA Venous pH obtained during routine blood draws can be used to avoidABGs

Decreased PCO2 reflects respiratory compensation formetabolic acidosis

Widening of anion gap is superior to pH or bicarbonateconcentration aloneWidening is independent of potentially masking effects

concurrent with acid base disturbances 21


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Potassium Total body potassium is depleted by renal losses

Measured levels usually normal or elevated

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Sodium

Osmotic diuresis leads to excessive renal losses of NaClin urine

Hyperglycemia artificially lowers the serum sodiumlevels

Two corrections: Standard-1.6 mEq added to sodium loss for every 100 mg of

glucose over 100 mg/dL

True-2.4 mEq added for blood glucose levels greater than 400mg/dL

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Symptoms of DKAAbdominal pain

Anorexia

Dehydration

Fuity breath

Kussmauls

Hypotension

N&V

Polyuria

Somnolence

TachycardiaThirst

Visual disturbances

Warm, dry skinWeakness

Wt. loss

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Electrolyte Loss: Osmotic diuresis contributes to urinary losses and

total body depletion of:

Phosphorus

Calcium

Magnesium

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Other values elevated: Creatinine Some elevation expected due to prerenal azotemia May be factitiously elevated if laboratory assays for Cr and Acetoacetate interfere

LFTs

Due to fatty infiltration of the liver which gradually corrects as acidosis is treated

CPK Due to volume depletion

Amylase

WBCs Leukocytosis often present due to hemoconcentration and stress response Absolute band count of 10,000 microL or more reliably predicts infection in this

population

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ECG changes Underlying rhythm is sinus tachycardia

Changes of hypo/hyperkalemia

Transient changes due to rapidly changingmetabolic status

Evaluate for ischemia because MI may precipitateDKA

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Differential Diagnosis Any entity that causes a high-anion-gap metabolic acidosis

Alcoholic or starvation ketoacidosis Uremia Lactic acidosis Ingestions (methanol, ethylene glycol, aspirin)

If ingestion cannot be excluded, serum osmolarity or drug-level testingis required

Patients with hyperosmolar non-ketotic coma tend to: Be older Have more prolonged course and have prominent mental status

changes Serum glucose levels are generally much higher (>600 mg/dL) Have little to no anion-gap metabolic acidosis

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Studies Diagnosis should be suspected at triage

Aggressive fluid therapy initiated prior to receiving lab results

Place on monitor and have one large bore IV with NS running

Rapid acucheck, urine dip and ECG

CBC

Electrolytes, phosphorus, magnesium, calcium

Blood cultures

ABG optional and required only for monitoring and diagnosis ofcritically ill Venous pH (0.03 lower than arterial pH) may be used for critically ill

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Assessment DKA Hyperglycemia

Hyperosmolality

Dehydration Electrolyte imbalances

Metabolic acidosis

Hypoglycemia

Fluid overload

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Treatment Goals:Volume repletion

Reversal of metabolic consequences of insulininsufficiency

Correction of electrolyte and acid-base imbalances

Recognition and treatment of precipitating causes

Avoidance of complications

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Intervention

Rehydrate Reverse shock

Give Potassium

Corret pH

Give insulin

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Treatment Order of therapeutic priorities is volume first, then insulin

and/or potassium, magnesium and bicarbonate

Monitor glucose, potassium and anion gap, vital signs, level ofconsciousness, volume input/output until recovery is wellestablished

Need frequent monitoring of electrolytes (every 1-2 hours) tomeet goals of safely replacing deficits and supplying missinginsulin

Resolving hyperglycemia alone is not the end point of therapy Need resolution of the metabolic acidosis or inhibition of ketoacid

production to signify resolution of DKA Normalization of anion gap requires 8-16 hours and reflects clearance of

ketoacids

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Fluid Administration Rapid administration is single most important step in treatment

Restores: Intravascular volume Normal tonicity

Perfusion of vital organs

Improve glomerular filtration rate

Lower serum glucose and ketone levels

Average adult patient has a 100 ml/Kg (5-10 L) water deficit and asodium deficit of 7-10 mEq/kg

Normal saline is most frequently recommended fluid for initial volumerepletion

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IV Fluids in DKA Hour 1

N/S or Ringers lactate (15-20ml/kg) Hour 2

Continue fluid, consider half-strength NS

Hour 3

Reduce fluid intake to 7.5ml/kg, use half-strength NS

Hour 4

Consider urine output in adjusting f luids

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Fluid Administration Recommended regimen:

First L of NS within first 30 minutes of presentation First 2 L of NS within first 2 hours

Second 2 L of NS at 2-6 hours Third 2 L of NS at 6-12 hours

Above replaces 50% of water deficit within first 12

hours with remaining 50% over next 12 hours

Glucose and ketone concentrations begin to fallwith fluids alone

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Fluid AdministrationAdd D5 to solution when glucose level is between

250-300 mg/dL

Change to hypotonic NS or D5 NS if glucosebelow 300 mg/dL after initially using NS

If no extreme volume depletion, may manage with

500 ml/hr for 4 hours May need to monitor CVP or wedge pressure in the

elderly or those with heart disease and may risk ARDSand cerebral edema

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Correct pH/Give Insulin Give IV Insulin

Give Regular Insulin only Initial bolus IV (0.15u/kg)

Then Regular Insulin IV drip

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Insulin Ideal treatment is with continuous IV infusion of small

doses of regular insulin

More physiologic

Produces linear fall in serum glucose and ketone bodylevels

Less associated with severe metabolic complicationssuch as hypoglycemia, hypokalemia andhypophosphatemia

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Insulin Recommended dose is 0.1 unit/kg/hr

Effect begins almost immediately after initiation ofinfusion

Loading dose not necessary and not recommended in

children

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Insulin Need frequent glucose level monitoring

Incidence of non-response to low-dose continuousIV administration is 1-2%

Infection is primary reason for failure

Usually requires 12 hours of insulin infusion oruntil ketonemia and anion gap is corrected

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Potassium Replacement in DKA

Look at EKG Replacement is based on plasma potassium level

Recheck potassium q 2 hours

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Potassium Patients usually with profound total body hypokalemia

3-5 mEq/kg deficient

Created by insulin deficiency, metabolic acidosis, osmotic

diuresis, vomiting

2% of total body potassium is intravascular

Initial serum level is normal or high due to: Intracellular exchange of potassium for hydrogen ions during acidosis Total body fluid deficit Diminished renal function Initial hypokalemia indicates severe total-body potassium depletion and

requires large amounts of potassium within first 24-36 hours

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Potassium During initial therapy the serum potassiumconcentration may fall rapidly due to:Action of insulin promoting reentry into cells Dilution of extracellular fluid

Correction of acidosis Increased urinary loss of potassium

Early potassium replacement is a standard modality of

care Not given in first L of NS as severe hyperkalemia may

precipitate fatal ventricular tachycardia and ventricularfibrillation

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Potassium Fluid and insulin therapy alone usually lowers thepotassium level rapidly For each 0.1 change in pH, serum potassium concentration changes

by 0.5 mEq/L inversely

Goal is to maintain potassium level within 4-5 mEq/L andavoid life threatening hyper/hypokalemia

Oral potassium is safe and effective and should be used assoon as patient can tolerate po fluids

During first 24 hours, KCl 100-200 mEq usually is required

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Phosphate Roll of replacement during treatment of DKA is

controversial

Recommended not treating until level less than 1mg/dL

No established roll for initiating IV potassiumphosphate in the ED

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Magnesium Osmotic diuresis may cause significant magnesium

depletion

Symptomatic hypomagnesemia in DKA is rare as isneed of IV therapy

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Bicarbonate Role in DKA debated for decades

No clinical study indicates benefit of treating DKA

with bicarbonate

Routine use of supplemental bicarbonate in DKA isnot recommended

Routine therapy works well without addingbicarbonate

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Complications and Mortality Complications related to acute disease

Main contributors to mortality are MI and infection

Old age, severe hypotension, prolonged and severe comaand underlying renal and cardiovascular disease

Severe volume depletion leaves elderly at risk forvascular stasis and DVT

Airway protection for critically ill and lethargic patientsat risk for aspiration

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Complications related to therapy Hypoglycemia

Hypophosphatemia

ARDS

Cerebral edema

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Complications related to therapy Cerebral edema

Occurs between 4 and 12 hours after onset of therapybut may occur as late as 48 hours after start treatment

Estimated incidence is 0.7 to 1.0 per 100 episodes of DKAin children

Mortality rate of 70%

No specific presentation or treatment variables predictdevelopment of edema

Young age and new-onset diabetes are only identifiedpotential risk factors

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Cerebral edema Symptoms include: Severe headache Incontinence Change in arousal or behavior Pupillary changes Blood pressure changes Seizures Bradycardia Disturbed temperature regulation

Treat with Mannitol Any change in neurologic function early in therapy should prompt

immediate infusion of mannitol at 1-2 g/kg

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Disposition Most require admission to ICU: Insulin drips

If early in the course of disease and can tolerate oralliquids, may be managed in ED or observation unitand discharged after 4-6 hours of therapy

Anion gap at discharge should be less than 20

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HHNKHyperglycemic, Hyperosmolar Noketotic Syndrome

Most commonly occurs in older adults with Type IIdiabetes

Always look for precipitating factors

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Factors Associated with HHNK

Drugs Procedures

Chronic illness

Acute illness

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Four Major Clinical Features

Severe hyperglycemia No or slight ketosis

Profound dehydration

Hyperosmolality

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Treatment

Similar to DKA

Find underlying cause

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Hyperosmolar Hyperglycemic State Syndrome of severe hyperglycemia, hyperosmolarity and

relative lack of ketonemia in patients with poorlyuncontrolled DM type II

ADA uses hyperosmolar hyperglycemic state (HHS) andhyperosmolar hyperglycemic non ketotic syndrome(HHNS) Both commonly used and appropriate

Frequently referred to as non ketotic hyperosmolar coma Coma should not be used in nomenclature

Only 10 % present with coma

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HHNS: Epidemiology HHNS is much less frequent than DKA

Mortality rate higher in HHNS

15-30 % for HHNS

5% for DKA

Mortality for HHNS increases substantially withadvanced age and concomitant illness

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Hyperosmolar Hyperglycemic State Defined by:

Severe hyperglycemia With serum glucose usually greater than 600 mg/dL

Elevated calculated plasma osmolality Greater than 315 mOsm/kg Serum bicarbonate greater than 15 Arterial pH greater than 7.3 Serum ketones that are negative to mildly positive

Values are arbitrary Profound metabolic acidosis and even moderate degrees

of ketonemia may be found in HHNS

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HHNS and DKA both Hyperglycemia

Hyperosmolarity

Severe volume depletion

Electrolyte disturbances

Occasionally acidosis

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HHNSAcidosis in HHNS more likely due to:

Tissue hypoperfusion

Lactic acidosis

Starvation ketosis

Azotemia

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HHNS and DKA Lipolysis DKA patients have much higher levels of lipolysis Release and subsequent oxidation of free fatty acids to

ketone bodies

hydroxybutyrate and Acetoacetate Contribute additional anions resulting in a more profound

acidosis

Inhibition of lipolysis and free fatty acidmetabolism in HHNS is poorly understood

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HHNS: Pathophysiology Three main factors: Decreased utilization of insulin Increased hepatic gluconeogenesis and glycogenolysis Impaired renal excretion of glucose

Identification early of those at risk for HHNS is mosteffective means of preventing serious complications

Must be vigilant on helping those who are non-ambulatorywith inadequate hydration status

Fundamental risk factor for developing HHNS is impairedaccess to water

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HHNS: Pathophysiology With poorly controlled DM II, inadequate utilization ofglucose due to insulin resistance results in hyperglycemia

Absence of adequate tissue response to insulin results inhepatic glycogenolysis and gluconeogenesis resulting infurther hyperglycemia

As serum glucose increases, an osmotic gradient isproduced attracting water from the intracellular space andinto the intravenous compartment

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HHNS: Pathophysiology Initial increase in intravascular volume is accompanied by atemporary increase in the GFR

As serum glucose concentration exceeds 180 mg/dL,capacity of kidneys to reabsorb glucose is exceeded andglucosuria and a profound osmotic diuresis occurs

Patients with free access to water are often able to preventprofound volume depletion by replacing lost water withlarge free water intake

If water requirement is not met, volume depletion occurs

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HHNS: Pathophysiology During osmotic diuresis, urine produced is markedly

hypertonic

Significant loss of sodium and potassium and modest loss ofcalcium, phosphate, magnesium and urea also occur

As volume depletion progresses, renal perfusion decreases andGFR is reduced

Renal tubular excretion of glucose is impaired which furtherworsens the hyperglycemia

A sustained osmotic diuresis may result in total body waterlosses that often exceeds 20-25% of total body weight or

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HHNS: PathophysiologyAbsence of ketosis in HHNS not clearlyunderstood Some degree of starvation does occur but a clinically

significant ketoacidosis does not occur

Lack of ketoacidosis may be due to: Lower levels of counter regulatory hormones

Higher levels of endogenous insulin that stronglyinhibits lipolysis

Inhibition of lipolysis by the hyperosmolar state

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HHNS: Pathophysiology Controversy how counter regulatory hormones glucagonsand cortisol, growth hormone and epinephrine play inHHNS Compared to DKA, glucagon and growth hormone levels are lower

and this may help prevent lipolysis

Compared to DKA, significantly higher levels of insulin arefound in peripheral and portal circulation in HHNS Though insulin levels are insufficient to overcome hyperglycemia,

they appear to be sufficient to overcome lipolysis

Animal studies have shown the hyperosmolar state andsevere hyperglycemia inhibit lipolysis in adipose tissue

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HHNS: Clinical Features Typical patient is usually elderly Often referred by a caretaker

Abnormalities in vital signs and or mental status

May complain of: Weakness Anorexia Fatigue Cough Dyspnea Abdominal pain

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HHNS Many have undiagnosed or poorly controlled type IIdiabetes

Precipitated by acute illness Pneumonia and urinary tract infections account for 30-50% of

cases

Noncompliance with or under-dosing of insulin hasbeen identified as a common precipitant also

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HHNS Those predisposed to HHNS often have some level ofbaseline cognitive impairment such as senile dementia Self-referral for medical treatment in early stages is rare

Any patient with hyperglycemia, impaired means ofcommunication and limited access to free water is at majorrisk for HHNS

Presence of hypertension, renal insufficiency orcardiovascular disease is common in this patientpopulation and medications commonly used to treat thesediseases such as blockers predispose the development ofHHNS

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HHNSAn insidious state goes unchecked Progressive hyperglycemia

Hyperosmolarity

Osmotic diuresis

Alterations in vital signs and cognition follow and

signal a severity of illness that is often advanced

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HHNS Causes Severe burns Renal insufficiency Peritoneal or hemodialysis Cerebrovascular events Rhabdomyolysis Commonly prescribed drugs that may predispose

to hyperglycemia, volume depletion or othereffects leading to HHNS

HHNS may unexpectedly be found in non-diabetics who present with an acute medical insultsuch as CVA, severe burns, MI, infection,pancreatitis or other acute illness

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HHNS: Physical findings Non-specific

Clinical signs of volume depletion: Poor skin turgor Dry mucus membranes Sunken eyeballs Hypotension

Signs correlate with degree of hyperglycemia and hyperosmolality andduration of physiologic imbalance

Wide range of findings such as changes in vital signs and cognition to clearevidence of profound shock and coma may occur

Normothermia or hypothermia is common due to vasodilation

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HHNS: Physical findings


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HHNS: Physical findings Seizures

Up to 15% may present with seizures

Typically focal

Generalized seizures that are often resistant toanticonvulsants may occur

Other CNS symptoms may include: Tremor

Clonus

Hyperreflexia Hyporeflexia

Positive plantar response

Reversible hemiplegia or hemisensory defects withoutCVA or structural lesion

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Degree of lethargy and coma is proportional to thelevel of osmolality

Those with coma tend to have:

Higher osmolality

Higher hyperglycemia Greater volume contraction

Not surprising that misdiagnosis of stroke or organic

brain disease is common in the elderly

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Laboratory tests Essential Serum glucose

Electrolytes

Calculated and measured serum osmolality

BUN

Ketones

Creatinine CBC

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Laboratory tests


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Laboratory tests

Consider Urinalysis and culture Liver and pancreatic enzymes Cardiac enzymes Thyroid function Coagulation profiles Chest x-ray ECG

Other CT of head LP Toxicology ABG

Of value only if suspicion of respiratory component to acid-base abnormality Both PCO2 and pH can be predicted from bicarbonate concentration obtained

from venous electrolytes

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Electrolyte abnormalities Electrolyte abnormalities usually reflect a contraction alkalosis due to profoundwater deficit

50% of patients with HHNS will have increased anion gap metabolic acidosis Lactic acidosis, azotemia, starvation ketosis, severe volume contraction

Acute or concurrent illnesses such as ischemic bowel will contribute anionssuch as lactic acid causing varying degrees of an anion gap metabolic acidosis

Initial serum electrolyte determinations can be reported as seemingly normalbecause the concurrent presence of both metabolic alkalosis and acidosis mayresult in each canceling out the others effect

Lack of careful analysis of serum chemistries may lead to delayed appreciationof the severity of underlying abnormalities, including volume loss

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Sodium


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Sodium Serum sodium is suggestive but not a reliable indicator of degree of volume contraction

Though patient is total body sodium depleted, serum sodium (corrected for glucoseelevation) may be low, normal or elevated

Measured serum sodium is often reported as factitiously low due to dilutional effect ofhyperglycemia

Need to correct the sodium level

Serum sodium decreases by 1.6 mEq for every 100 mg/dL increase in serum glucoseabove 100 mg/dL

Elevated corrected serum sodium during sever hyperglycemia is usually explainableonly by profound volume contraction

Normal sodium level or mild hyponatremia usually but not invariably suggests modestdehydration

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Osmolarity Serum osmolarity has also been shown to correlate with severity of

disease as well as neurologic impairment and coma

Calculated effective serum osmolarity excludes osmotically

inactive urea that is usually included in laboratory measures ofosmolari

Normal serum osmolarity range is approximately 275 to 295mOsm/kg

Values above 300 mOsm/kg are indicative of significanthyperosmolarity and those above 320 mOsm are commonlyassociated with alterations of cognitive function

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Potassium


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Hypokalemia is most immediate electrolyte based risk and should beanticipated

Total body deficits of 500-700 mEq/l are common

Initial values may be reported as normal during a period of severe volumecontraction and with metabolic acidosis when intravascular hydrogen ionsare exchanged for intracellular potassium ions

Presence of acidemia may mask a potentially life-threatening potassiumdeficit

As intravascular volume is replaced and acidemia is reversed, potassiumlosses become more apparent

Patients with low serum potassium during the period of severe volumecontraction are at greatest risk for dysrhythmia

Importance of potassium replacement during periods of volume repletionand insulin therapy cannot be overemphasized

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Phosphate Hypophosphatemia may occur during periods of prolonged hyperglycemia

Acute consequences such as CNS abnormalities, cardiac dysfunction, andrhabdomyolysis are rare and are usually if level is


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Treatment Improvement in tissue perfusion is the key to effective recovery

Treat hypovolemia, identify and treat precipitating causes,correct electrolyte abnormalities, gradual correction ofhyperglycemia and osmolarity

Cannot overstate importance of judicious therapeutic plans thatadjusts for concurrent medical illness such as LV dysfunction orrenal insufficiency

Due to potential complications, rapid therapy should only bereserved for potentially life-threatening electrolyteabnormalities only

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Fluid resuscitation Initial aim is reestablishing adequate tissue perfusion anddecreasing serum glucose

Replacement of intravascular fluid losses alone can account forreductions in serum glucose of 35-70 mg/hr or up to 80 % of

necessary reduction

Average fluid deficit is 20-25% of total body water or 8-12 L

In elderly 50% of body weight is due to total body water

Calculate the water deficit by using patients current weight inkilograms and normal total body water

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Fluid resuscitation One-half of fluid deficits should be replaced over the initial 12hours and the balance over the next 24 hours when possible

Actual rate of fluid administration should be individualized foreach patient based on presence of renal and cardiac impairment

Initial rates of 500-1500 ml/hr during first 2 hours followed byrates of 250-500 ml per hour are usually well tolerated Patients with cardiac disease may require a more conservative rate of

volume repletion

Renal and cardiovascular function should be carefully monitored

Central venous and urinary tract catheterization should beconsidered

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Fluid resuscitation Rate of fluid administration may need to be limited in children

A limited number of reports of cerebral edema occurring during or soon afterthe resuscitation phase of patients with both DKA and HHNS have beendescribed

Most cases have occurred in children with DKA and mechanism is unclear

One review showed cerebral edema was found with similar frequency beforetreatment with replacement fluids

New study shows rehydration of children with DKA during first 4 hours at arate greater than 50 mL/kg was associated with increased risk of brainherniation

Little credible data on incidence or clinical indicators that may predispose tocerebral edema in HHNS patients

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Fluid resuscitation Current recommendations based on available data include limiting rate ofvolume depletion during first 4 hours to


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Potassium Potassium deficits are most immediate electrolyte-based risk for a

bad outcome

On average potassium losses range from 4-6 mEq/kg though maybe as high as 10mEq/kg of body weight

Initial measurements may be normal or even high with acidemia

Patients with levels


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Potassium When adequate urinary output is assured, potassiumreplacement should begin

Should replace at 10-20 mEq/hr though if life threateningmay require 40 mEq/hr

Central line needed if given more than 20 mEq/hr

Some believe potassium through central line poses risk for

conduction defects and should be avoided if good peripheralline sites are available

Monitoring of serum potassium should occur every hour untila steady state has been achieved

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Sodium Sodium deficits replenished rapidly since given NS or NS

during fluid replacement

Phosphate and Magnesium should be measured

Current guideline recommend giving 1/3 of potassium neededas potassium phosphate to avoid excessive chlorideadministration and to prevent hypophosphatemia

Unless severe, alleviation of hypophosphatemia orhypomagnesemia should occur after the patient is admitted intothe ICU setting

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Insulin Volume repletion should precede insulin therapy

If given before volume repletion, intravascular volume is furtherdepleted due to shifting of osmotically active glucose into theintracellular space bringing free water with it and this may

precipitate vascular collapse

Absorption of insulin by IM or SC route is unreliable in patientswith HHNS and continuous infusion of IV insulin is needed

No proven benefit to bolus of insulin

Continuous infusion of 0.1U/kg/hour is best

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Insulin

Want one unit of regular insulin for every mL of NS in infusion

Steady states utilizing infusion pumps occur within 30 minutes ofinfusion

Decrease plasma glucose by 50-75 mg/dL per hour along with adequatehydration

If adequate hydration, may double infusion rate until 50-75 mg/dL/hris achieved

Some patients are insulin resistant and require higher doses

Once level less than 300 mg/dL, should change IV solution to D5 NSand insulin infusion should be reduced to half or 0.05 U/kg/hr.

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Questions 1. T/F: The venous pH is just as helpful as arterial pH in patients with DKA and

may be obtained during routine blood draws.

2. T/F: Alcoholic ketoacidosis is usually seen in chronic alcoholics but may beseen in first time drinkers who binge drink, especially in those with volumedepletion from poor oral intake and vomiting.

3. T/F: In treating DKA, the order of therapeutic priorities is volume first, theninsulin and/or potassium, magnesium and bicarbonate.

4. T/F: DKA patients have much higher levels of lipolysis, resulting in releaseand subsequent oxidation of free fatty acids to ketone bodies contributing

additional anions resulting in a more profound acidosis than in HHNS.

5. T/F: Volume repletion should precede insulin therapy in HHNS

Answers:

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Hypoglycemia

Also known as insulin reaction or hypoglycemic

reaction

100

H l i


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Hypoglycemia

Weak, sweaty

Confused/irritable/

disoriented


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Risk Factors

Overdose of insulin

Omitting a meal

Overexertion

Nausea and vomiting

Alcohol intake

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Symptoms of Hypoglycemia

Adrenergic Shakiness

Irritability Nervousness Tachycardia Tremor Hunger Diaphoresis Pallor Paresthesias

Neuroglycopenic Headache

Mental illness Inability to concentrate Slurred speech Blurred vision Confusion Irrational behavior Lethargy LOC, coma, seizure

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Interventions

Mild

carbohydrate 10-15 gram

Moderate

20-30 gram of carbs

Glucagon, 1 mg SC or IM

Severe 50% dextrose 25 g IV

Glucagon 1 mg IM or IV

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Helping others is good, teaching

them to help themselves is better.

George Orwell

Slides current until 2008


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Chronic Complications of DMMacrovascular

Retinopathy , Cataract

Nephropathy

Peripheral Neuropathy

Autonamic Neuropathy

Foot Disease


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Macrovascular

Coronary Circulation

Cerebral Circulation

Peripheral Circulation


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RETINOPATHY- PathophysiologyHyperglycaemia

increased Retinal blood flow

Retinal endothelial cells & pericytes

Impaired vascular autoregulation

Dilated capillaries + production of vasoactivesubsdtances +endothelial cell proliferation

Capillary closureCHRONIC RETINAL HYPOXIA

Vascular endothelial growth factor(VEGF)

Acute Complications of DM

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