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Hyperosmolar 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 - such as illness, poor heart conditions

- They prone to develop because of physical form of stress

(synthesis of blood sugar) (cortisol is a stress hormone)

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

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 Take certain medications—that can cause the syndrome

Symptoms

 High blood sugar level

 Confusion, hallucinations, drowsiness or passing out

 Dry mouth and extreme thirst that may eventually get 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:

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 insulin regimen,

 missed dosages of oral hypoglycemic agents,

 overconsumption of carbohydrate-rich diet,

 simultaneous use of medications

History and Physical Examination: System based approach

 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; presence of glycosuria and ketonuria

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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.

 Secure the airway if the Glasgow coma score is less than 8.

 Aggressive hydration with isotonic fluid with electrolyte replacement

 Potassium replacement should be started when the serum potassium is between 4 to 4.5
mmol/L.

Potential Complications

 Seizures

 Coma

 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% NS to hydrate the cells.
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 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.

Preventiion

 Checking blood sugar frequently

 Taking insulin and other diabetes medications as directed by the doctor

 Following a healthy diet

 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.

Liver Failure

Description:

 This refers to a condition in which the liver isn’t working well enough to perform its functions
(for example, manufacturing bile and ridding the body of harmful substances).

Pathophysiology

 Irrespective of the cause of liver injury, inflammation results in damage to hepatocytes, known
as “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:

Acute Liver Failure

 It results in a rapid deterioration of liver function in a person without prior liver disease.

 Loss of liver function that occurs rapidly

 The cellular insult results in massive cell necrosis leading to a multiorgan dysfunction.

Chronic Liver Failure

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 A slow deterioration that evolves over years leading to cirrhosis.

 Liver dysfunction potentially can be reversed early as the liver has a regenerative capability

Etiology/Causes-Acute Liver Failure

 Acetaminophen overdose. Taking too much acetaminophen (Tylenol, others)

 Prescription medications. Some prescription medications such as antibiotics

 Herbal supplements. Herbal drugs and supplements such as kava and ephedra

 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

 Autoimmune disease: autoimmune hepatitis

 Diseases of the veins in the liver: Budd-Chiari syndrome

 Metabolic disease: Wilson's disease and acute fatty liver of pregnancy

 Cancer. Cancer that either begins in or spreads in the liver

 Shock. Overwhelming infection (sepsis) and shock can severely impair blood flow to the liver

 Heat stroke. Extreme physical activity in a hot environment

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

Clinical Manifestations-Acute Liver Failure

 feeling unwell (malaise)

 feeling tired or sleepy

 nausea or vomiting

 abdominal pain or swelling

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 yellowing of the skin and eyes (jaundice)

 feeling confused or disoriented

The early symptoms of chronic liver failure may include:

 feeling tired or fatigued

 loss of appetite

 nausea or vomiting

 mild abdominal discomfort or pain

Symptoms that can indicate the advanced stages of chronic liver failure include:

 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.
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• 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

 Monitor fluid balance.

 Assist with paracentesis that may be instituted to reduce ascites. .

Supporting Cardiopulmonary Status

 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 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.

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 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.

After liver transplantation the nurse must:

 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

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• 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.