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HYPEROSMOLAR  Dry mouth and extreme thirst that may eventually get
HYPERGLYCEMIC SYNDROME
Description:
 It occurs when a person’s blood glucose (sugar)
levels are too high for a long period, leading to severe
dehydration (extreme thirst) and confusion. Also
known as: Diabetic HHS, Diabetic hyperosmolar
syndrome
Commonly affected Individuals
 Older population
 Individuals with health issues
What causes hyperosmolar hyperglycemic syndrome
(HHS)?
 It occurs when the blood sugar of a person with
diabetes becomes too high (hyperglycemia) for a
long time.
 The extra sugar is passed into the urine, which causes
the person to urinate frequently.
 As a result, the patient loses a lot of fluid, which can
lead to severe dehydration (extreme thirst).
HHS usually develops in people who do not have their type
2 diabetes under control and they:
 Have an illness or infection
 Stop taking medication
 Have a heart attack or stroke
 Take certain medications—
that can cause the syndrome
Symptoms
 High blood sugar level
 Confusion, hallucinations, drowsiness or passing out
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better
 Frequent urination
 Fever over 100.4 degrees Fahrenheit
 Blurred vision or loss of vision
 Weakness or paralysis
Pathophysiology:
 The hallmark of both conditions is the deficiency
of insulin. As a consequence of deficiency of this
key hormone, there is a decrease in glucose
utilization by the peripheral tissue causing
hyperglycemia.
 The peripheral tissues enter a state of “starvation”.
 The release of counterregulatory hormones like the
glucagon, growth hormone, cortisol, and
catecholamines stimulates gluconeogenesis and
glycogenolysis.
 This creates a system of vicious cycle where there is
an increased level of glucose in the serum but
decreased uptake by the peripheral tissues for tissue
metabolism.
 The serum osmolality is determined by the formula
2Na + Glucose /18 + BUN / 2.8.
 The resultant hyperglycemia increases the serum
osmolarity to a significant degree. The glucose level
in HHS is usually above 600 mg/dL.
 Hyperglycemia also creates an increase in the
osmotic gradient with free water drawn out of the
extravascular space due the increased osmotic
gradient.
 Free water with electrolytes and glucose is lost via
urinary excretion producing glycosuria causing
moderate to severe dehydration.
History and Physical Examination
 Should be focused on the following:
 insulin regimen,
 missed dosages of oral hypoglycemic agents,
 overconsumption of carbohydrate-rich diet,
 simultaneous use of medications
History and Physical Examination:
System based approach
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 GENERAL APPEARANCE: generally ill-appearing
with altered mental status
 CARDIOVASCULAR: Tachycardia, orthostatic
hypotension, weak and thready pulse
 RESPIRATORY: Rate can be normal, but tachypnea
might be present if acidosis is profound
 SKIN: Delayed capillary refill, poor skin turgor, skin
tenting might not be present even in severe dehydration
because of obesity
 GENITOURINARY: Decreased urine output
 CENTRAL NERVOUS SYSTEM (CNS): Focal
neurological deficit, lethargy with low Glasgow Coma
Score and in severe cases of HHS.
Diagnostics / Laboratory Examinations
 Glucose: greater than 600 mg/dL
 Serum Osmolality: very high, levels between 320 to
400mOsm/kg
 Sodium: falsely low (pseudohyponatremia)
 Potassium: might be high or low
 Bicarbonate: close to normal in HHS, around 8 to 12
mmol/ usually very low.
 Magnesium: might be low
 Ketones: Ketonemia is very minimal
 Arterial Blood Gases: above or around 7.30
 Renal Function: BUN and creatine levels are usually
elevated reflecting prerenal azotemia
 Serum Enzymes: usually high from hemoconcentration
and dehydration
 Complete Blood Count: white blood cell count,
hemoglobin and hematocrit levels are elevated
 Urine Analysis: specific gravity is high; presence of
glycosuria and ketonuria
Treatment / Management
 Consultations with an endocrinologist and an intensive
care specialist are recommended.
 Appropriate resuscitation with attention to the principle
of Airway, Breathing, Circulation (ABC) should be
initiated.
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 Secure the airway if the Glasgow coma score is less
than 8.
 Aggressive hydration with isotonic fluid with
electrolyte replacement. (ISOTONIC because there is
no shifting of fluid in the extra and intra cellular
compartment)
 Potassium replacement should be started when the
serum potassium is between 4 to 4.5 mmol/L.
Potential Complications
 Seizures (brain irritation brought about by the
accumulation of substances / glucose…)
 Coma (because of increase in blood glucose level)
 Swelling of the brain
 Organ failure
 Death
Nursing Diagnoses:
• Risk For Fluid Volume Deficit related to decreased
intake of fluids due to diminished thirst sensation or
functional inability to drink fluids/excessive gastric
losses due to nausea and vomiting/hyperglycemia-
induced osmotic diuresis.
• Risk For Infection related to preexisting respiratory
infection, or UTI/high glucose levels/decreased
leukocyte function/changes in circulation.
• Deficient Knowledge maybe related to unfamiliarity
with the risk factors, treatment, and prevention of the
disease.
• Imbalanced Nutrition: Less Than Body
Requirements related to decreased oral
intake/hypermetabolic state: release of stress
hormones /insufficient insulin
Nursing Interventions
Goal: Hydrate, decrease blood glucose, monitor potassium
levels and for cerebral edema, correct acid-base imbalance.
 Administering IV fluids: (depending on MD order)
such as 0.9% Normal Saline (start out with a bolus of
this) and progress with 0.45% Normal Saline to
hydrate the cells. (when the glucose is around 250-300
mg/dL)
 Administered insulin REGULAR (only type given
IV) and make sure K+ is normal >3.3
 Watch potassium levels very closely because insulin
causes K+ to move back into the cell.
Prevention
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 Checking blood sugar frequently  Prescription medications. Some prescription
medications such as antibiotics.
 Taking insulin and other diabetes medications as
directed by the doctor  Herbal supplements. Herbal drugs and supplements
 Following a healthy diet such as kava and ephedra.

 Never drink alcohol on an empty stomach
 Getting more rest and checking blood sugar more
often when individuals are sick.
 Knowing the symptoms of HHS and getting help
right away.
 Hepatitis and other viruses. Hepatitis A, hepatitis B
and hepatitis E; Other viruses like Epstein-Barr
virus, cytomegalovirus and herpes simplex virus.
 Toxins: poisonous wild mushroom Amanita
phalloides and Carbon tetrachloride

Liver Failure 


Autoimmune disease: autoimmune hepatitis

Diseases of the veins in the liver: Budd-Chiari

syndrome
Description:
 Metabolic disease: Wilson's disease and acute fatty
 This refers to a condition in which the liver isn’t liver of pregnancy
working well enough to perform its functions (for
example, manufacturing bile and ridding the body of  Cancer. Cancer that either begins in or spreads in the
harmful substances). liver

 Shock. Overwhelming infection (sepsis) and shock

Pathophysiology can severely impair blood flow to the liver
 Irrespective of the cause of liver injury, inflammation
 Heat stroke. Extreme physical activity in a hot
results in damage to hepatocytes, known as
environment
“hepatitis.”

 Injured areas are surrounded by scar tissues leading
to fibrosis, and after a period of time progressive
fibrosis results in cirrhosis or replacement of the
normal hepatic tissue with fibrotic tissue.
Types:
1. ACUTE LIVER FAILURE
Etiology / Causes-Acute Liver Failure
 Chronic hepatitis B or C infection
 Alcohol-related liver disease
 Nonalcoholic fatty liver disease
 Autoimmune hepatitis
 Diseases that affect the bile ducts, such as cholangitis

 It results in a rapid deterioration of liver function in a

Clinical Manifestations - Acute Liver Failure
person without prior liver disease.
 feeling unwell (malaise)
 Loss of liver function that occurs rapidly  feeling tired or sleepy
 nausea or vomiting
 The cellular insult results in massive cell necrosis  abdominal pain or swelling
leading to a multiorgan dysfunction.  yellowing of the skin and eyes (jaundice)
 feeling confused or disoriented
2. CHRONIC LIVER FAILURE

 A slow deterioration that evolves over years leading The early symptoms of chronic liver failure may
to cirrhosis. include:

 Liver dysfunction potentially can be reversed early as  feeling tired or fatigued

the liver has a regenerative capability  loss of appetite
 nausea or vomiting
Etiology / Causes - Acute Liver Failure  mild abdominal discomfort or pain

 Acetaminophen overdose. Taking too much Symptoms that can indicate the advanced stages of
acetaminophen (Tylenol, others). chronic liver failure include:

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 yellowing of the skin and eyes (jaundice)
 easy bruising or bleeding
 feeling confused or disoriented
 buildup of fluid in your abdomen, arms, or legs
 darkening of your urine
 severe skin itching
Stages of Liver Failure
 Inflammation: the liver is enlarged or inflamed.
 Fibrosis. Scar tissue begins to replace healthy tissue
in the inflamed liver.
 Cirrhosis. Severe scarring has built up, making it
difficult for the liver to function properly
 End-stage liver disease (ESLD). Liver function has
deteriorated to the point where the damage can’t be
reversed other than with a liver transplant.
 Liver cancer. The development and multiplication of
unhealthy cells in the liver can occur at any stage of
liver failure, although people with cirrhosis are more
at risk.
Diagnostic Assessment
 Liver blood tests (ALT/AST). Assess the levels of
various proteins and enzymes in the blood that can be
an indicator of the liver functions.
 Blood Tests. A complete blood count (CBC) or test
for viral hepatitis or genetic conditions that can cause
liver damage.
 Imaging tests. Imaging technology such
as ultrasound, CT scan, or MRI scan is done to
visualize the liver.
 Biopsy. Taking a tissue sample from the liver to see
if scar tissue is present and can also aid in diagnosing
what may be causing the condition.
Principles of Management
Decreasing Metabolic Requirements of the Liver
 Place the patient on bed-rest to decrease the
metabolic needs of the liver
 Institute measures to prevent skin breakdown.
 Monitor drugs that are metabolized or detoxified by
the liver, especially narcotics and sedatives
Supporting Cardiopulmonary Status
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 Monitor fluid balance. (to determine if there is water
retention / water deficit)
 Assist with paracentesis that may be instituted to
reduce ascites.
 Monitor respiratory status and correlate with arterial
blood gas results.
 Administer oxygen as ordered.
 Administer sedatives and analgesics cautiously.
 Assist the patient with maneuvers to improve
oxygenation.
Support Hematologic, Nutritional, and Metabolic Functions
of the Liver
 Monitor for signs of bleeding (eg, gastric contents,
stools, urine) and test for occult blood.
 Administer blood and blood products as ordered.
 Institute measures for variceal bleeding (bleeding of
varices found throughout the GI tract) as needed,
including beta blockers.
 Institute measures to provide for safety and to
minimize tissue trauma.
 Provide frequent small meals and a bedtime snack
containing carbohydrate to prevent muscle wasting.
 Monitor for signs and symptoms of infection.
Preventing and Treating Complications
 Observe for changes in mentation.
 Administer cleansing enemas and cathartics to keep
the bowel empty.
 Monitor patient response to therapy through
neurologic assessments and serum ammonia levels.
 Monitor the use of medications metabolized by the
liver.
 Institute protocols for acute upper GI hemorrhage due
to variceal rupture.
Surgical Management
Liver Transplantation
 This involves removing the diseased liver and
replacing it with a liver from a healthy donor.
Nursing care postoperative:
After liver transplantation the nurse must:
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 Assess the patient for such complications as
bleeding, infection, and rejection.

 Monitor the patient’s temperature, urine output,

neurologic status and hemodynamic pressures.

 Provide education about immunosuppressive drugs.

Nursing Management
 Monitor level of consciousness, blood pressure,
volume status, blood and coagulation tests, and signs
and symptoms.
 Keep the head of the bed elevated 30 degrees, with
the patient’s head in the neutral position.
 Decrease stimulation, such as frequent suctioning.
 Stay alert for hypercapnia and hypoxia; correct these
conditions as indicated and ordered.
 Manage fever aggressively with a fan, cooling
blanket, or both.
 Watch for signs and symptoms of infection and
possible sepsis; administer antibiotics, as needed and
ordered.
 Maintain strict glucose monitoring for possible
hypoglycemia or hyperglycemia.
 Provide nutritional support as ordered

Prevention
Chances of developing liver failure can be reduced by:

 Being vaccinated for hepatitis B

 Cutting down on alcohol
 Maintaining a healthy weight and active lifestyle
 Following directions when using medications like
acetaminophen (Tylenol®)
 Having a physical examination every year (at least)
with a primary care provider, with screening
for obesity, high cholesterol, high blood pressure and
diabetes

References:

Terry, C. and Weaver, A. (2011). Critical care nursing

deMYSTiFieD. The McGraw-Hill Companies, Inc

Mortone, P and Fontaine, D. (2013). Critical care nursing a holistic

approach. Lippincott Williams &

Wilkins Smeltzer, S.C., et.al. 2010. Brunner & Suddarth’s Textbook

of medical-surgical nursing, 12th edition. Philadelphia, PA:
Lippincott Williams & Wilkins.

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