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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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h i l fi di
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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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HHNS: Physical findings
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HHNS: Physical findings
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
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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)