hhns r.kalaivani

8/11/2019 HHNS R.kalaivani

1/14

HyperosmolarHyperglycemic Nonketotic

syndrome

KALAIVANI RAMACHANDRAN12 1 9 52


2/14

HHNS

DefinitionSevere hyperglycemia w/

Serum glucose >600mg/dL

Plasma osmolarity > 315mOsm/kg Bicarb > 15 Arterial pH > 7.3 Serum ketones - negative or mildly elevated

EpidemiologyHHNS occurs less often than DKA, but has amuch higher mortality.


3/14


4/14

Pathophysiology

HHNS is attributed to three factors1. Decreased insulin utilization2. Increased gluconeogenesis & glycogenolysis3.

Impaired renal excretion of glucose End result - hyperglycemia and volume

depletion through osmotic diuresis. Total body water losses can reach 8-12 liters

Lack of ketoacidosis in HHNS attributed to1. Lower levels of counterregulatory hormones2. High levels of endogenous insulin inhibiting lypolysis3. Hyperosmolar state inhibiting lypolysis


5/14

Clinical FeaturesHISTORY AND PRESENTATION-

Known history of diabetes mellitus (DM), whichis usually type 2

Patients may complain of increasing thirst,polydipsia, polyuria, weight loss, and weakness

A wide variety of focal and global neurologicchanges may be present, including drowsinessand delirium to hemiparesis and coma


6/14

PHYSICAL EXAMINATION-

Examine the patient for evidence of HHS, focusing onhydration status, mentation(skin tugor), and signs ofpossible underlying causes, such as a source ofinfection.

Tachycardia is an early indicator of dehydration;hypotension is a later sign suggestive of profounddehydration due to volume loss secondary to osmoticdiuresis.

Body weight is the single most important measurementin assessing the degree of hydration. For every 1 L ofbody fluids lost, 1 kg of body weight is lost.


7/14


8/14

Treatment

Key is to improve tissue perfusionFluid resuscitation

NS preferred

Initial rates of 500-1500 mL/h during first two hrs.More conservative therapy for pts w/ cardiac ds.Once hypotension, tachycardia, and urinary outputimprove fluid can be changed to 1/2NS.D5 NS can be used once serum glucose reaches250-300mg/dL.


9/14

Treatment

ElectrolytesK+

Initial levels may be normal or high in the presence ofacidemia

Levels < 3.3mEq/L represents severe deficit and are at riskfor dysrhythmias.

Replacement can begin once urinary output is assured.Replace at a rate of 10-20mEq/h.

Na+ Replaced rapidly w/ the amount of NS required for fluid

resuscitation.

Mag and Phos No current guidelines for random replacement in the ED.


10/14

Treatment

Insulin As in DKA IV administration preferred over IMor SubQ due to poor adsorption.IV infusion at rate of 0.1 units/kg/h R insulinLoading dose is optionalOnce serum glucose reaches 250-300mg/dL

fluid can be to D5 1/2NS and insulin can bedecreased to 0.05units/kg/h.


11/14

COMPLICATIONS:Cerebral edema may occur from rapid lowering of glucose levels and anensuing rapid drop in plasma osmolarity

Acute respiratory distress syndrome, PE, MI, or pneumonitis that hasworsened with rehydration-rapid correction of hyperglycemia andhyperosmolarity gives rise to pulmonary edema

Vascular complications like hypotension and hyperviscosity of the blood,both of which predispose patients to thromboembolic disease of thecoronary, cerebral, pulmonary, and mesenteric beds


12/14

Patient Education:

Diabetic teaching, provided both in the hospital and after discharge by the

primary care physician

A certified diabetes educator should instruct all patients on management ofsick days

What warning signs should the patient keep in mind?

Dry, parched mouth Extreme thirst (although this may gradually disappear) Warm, dry skin that does not sweat

High fever (over 101 degrees Fahrenheit, for example) Sleepiness or confusion Loss of vision Hallucinations (seeing or hearing things that are not there) Weakness on one side of the body


13/14

Prognosis

The overall mortality rate of HHS is more than ten times

that of diabetic ketoacidosis, chiefly because of

its higher incidence in older patients, who may havecompromised cardiovascular systems or associated

major illnesses and whose dehydration is oftenexcessive because of delays in recognition andtreatment.

When prompt therapy is instituted, the mortality rate canbe reduced from nearly 50% to that related to theseverity of coexistent disorders.


14/14

hhns r.kalaivani

Documents