RESPONSES TO

METABOLIC-GI
AND LIVER
ALTERATIONS

SHARED BY:
MICHAEL P. TUYAY
GENERAL ASSESSMENT
*Assess patient’s physical & psychological statuses & interpret lab data.
A. Altered Gastrointestinal Function
1. General Nutritional Status Interview
 Should begin with questions regarding client’s dietary habits
 Questions should elicit information about average daily intake of food and liquids,
types and quantities consumed, where and when food is eaten, and any conditions or diseases that
affect intake or absorption
 What questions do you ask?
o Food intake history, Time, Food/drink, Amount, Method of preparation
GENERAL ASSESSMENT
*Assess patient’s physical & psychological statuses & interpret lab data;
A. Altered Gastrointestinal Function
2. Health History
 Elicit a description of present illness and chief complaint or symptoms through
COLDSPA o Characteristics, onset, location, duration, severity, precipitating & alleviating factors
 Family history, prenatal history, medications, use of tobacco and alcohol
 Complete nutritional history including 24-hour dietary intake
GENERAL ASSESSMENT
*Assess patient’s physical & psychological statuses & interpret lab data;
B. Focused Assessment of Clients with Hepato-Biliary & Pancreatic Disorders
1. Health History
 Elicit description of present illness and chief complaint o Onset, course, duration,
location, and precipitating and alleviating factors o Cardinal signs and symptoms indicating
altered hepatic, biliary, and pancreatic function include:  Jaundice, pruritus
 Jaundice can produce pruritus due to impaired bile-acid excretion 
Changes in urine and stool color
 Vague to severe abdominal pain especially after eating fatty foods 
Abdominal tenderness and distention
 Easy bruising and bleeding
GENERAL ASSESSMENT
*Assess patient’s physical & psychological statuses & interpret lab data;
B. Focused Assessment of Clients with Hepato-Biliary & Pancreatic Disorders
1. Health History
 Alcohol consumption
 Diet high in fat
 Infectious agents (transmitted thru nonsterile needle puncture, unprotected sexual
activity, ingestion of potentially contaminated food, etc)
 Recent blood transfusions
 Medications and herbal remedies
o Some sample drugs with high potential for hepatotoxicity:
 NSAIDS – such as ibuprofen, acetaminophen
 Antiseizure meds – phenytoin, valproic acid
 TB drugs – isoniazid, pyrazinamide
PHYSICAL ASSESSMENT
*Patient lies supine, knees flexed, slightly for inspection, auscultation, percussion & palpation of
the abdomen
PHYSICAL ASSESSMENT
1. Inspection
- Performed first noting any skin changes, nodules, skin lesions, scarring and/or
discolorations - Lesions
are of particular importance because GI diseases often produce skin changes
- Inspect contour & symmetry of the abdomen noting for any localized bulging &
distention
o Expected contours of the anterior abdominal wall: flat, rounded, or scaphoid
- Nsg priorities during inspection:
o Focuses on oral cavity, skin over the abdomen, & shape of the abdomen

 Skin, mucosa & sclerae: jaundice, petechiae or ecchymotic areas, spider angiomas, palmar erythema 
Extremities: muscle atrophy, edema, skin excoriation s/t scratching  Abdomen:
contour, girth, pigmentation, color, scars, striae, visible masses, peristalsis & pulsations  Cognitive & Neurologic Status
PHYSICAL ASSESSMENT
2. Auscultation
- Always precedes percussion & palpation because this may alter bowel sounds -
Determines character, location, frequency of bowel sounds -
Identifies vascular sounds -
Bowel sounds are using the diaphragm of the stethoscope for soft clicks & gurgling sounds
- Frequency &
character of the sounds are usually heard as clicks & gurgles that occur irregularly
 Auscultate bowel sounds
before percussion and palpation (5-30 clicks/min – using diaphragm of stethoscope for 5 minutes)
 Normal bowel sounds occur 5-30 times
a min or every 5-15 seconds  Auscultate in all abdominal quadrants o Auscultate for
vascular sounds (e.g. bruits, hepatic friction rub)
PHYSICAL ASSESSMENT
3. Percussion
- Size, density of the abdominal organs
- Detect of air-filled, fluid-filled or sold masses
 Percuss all 4 quadrants noting tympany and dullness

4. Palpation
- Performed last so that the sounds from palpation aren’t auscultated
 Palpate deeply over all 4Qs for any masses and note location, size and shape, pulsation
 Palpate liver, spleen, kidneys, and aorta for enlargement
 Always palpate tender areas last
DIAGNOSTIC ASSESSMENT
A. NON-INVASIVE
1. GUAIAC TEST (STOOL FOR OCCULT BLOOD): Detect GI bleeding (GI cancer)
2. HEPATOBILIARY SCAN: Radioactive materials=size and shape of liver
tissue/visualize replacement of liver tissue with scars, cysts and tumor
3. Radionuclide Imaging or Cholecystography : images of the gallbladder and biliary tract
4. Barium Swallow (Upper GIT study/series): drinks barium sulfate (BaSO4)=to visualize
the esophagus, stomach, duodenum and jejunum
5. Lower GI study/series (Barium enema): detecting bowel obstruction and cause of
diarrhea and constipation
6. Capillary Blood Glucose Monitoring: monitoring blood glucose patterns
Normal blood is sugar is defined as: (1) An FBS < 100 mg/dL (5.6 mmol/L), or (2) Random/casual blood glucose < 140
mg/dl (7.7mmol/L), or (3) 2-hr blood sugar in the 75gm OGTT < 140 mg/dl (7.7mmol/L) [Level 2, Grade B].
DIAGNOSTIC ASSESSMENT
B. INVASIVE
1. ESOPHAGOGASTRODUODENOSCOPY (EGD): Upper GI fibroscopy
2.ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY (ERCP):
Endoscopic visualization of common bile, pancreatic, and hepatic ducts
3. PERCUTANEOUS TRANSHEPATIC CHOLANGIOGRAPHY (PTC): Useful for
distinguishing jaundice caused by liver disease (hepatocellular jaundice) from that caused by
biliary obstruction, for investigating the gastrointestinal symptoms of a patient whose gallbladder
has been removed, for locating stones within the bile ducts, and for diagnosing cancer involving
biliary system
4. LIVER BIOPSY: Sampling liver tissue by needle aspiration for histologic analysis
5. SERUM BLOOD STUDIES: Liver function tests, Serum Proteins, Pigment Studies,
Serum Ammonia, Blood Coagulation Studies (PT, INR, PTT)
NURSING DIAGNOSES
- Acute/Chronic Pain related to Lesions Secondary to Increased Gastric secretions
- Imbalanced Nutrition: Less than Body Requirements related to Anorexia
- Impaired Comfort related to Pruritus
- Excess Fluid Volume related to Portal Hypertension
- Pain related to Liver Enlargement - High Risk for Ineffective Therapeutic Regimen related to
Lack of Knowledge
- Decreased Cardiac Output related to Alterations in Preload
- Deficient Fluid Volume related to Absolute Blood Loss - Anxiety related to Threat to Biologic,
Psychologic and or Social Integrity
- Hyperthermia related to Increased Metabolic Rate
PLANNING
 Administering Volume Replacement
 Controlling bleeding
 Maintaining surveillance for complications
 Administering fluids, insulin, and electrolytes
 Monitor Response to therapy
 Normalize body temperature
 Patient education
METABOLIC-
GI AND LIVER
ALTERATIONS
SHARED BY:
MICHAEL P. TUYAY
ACUTE GI BLEEDING
 Gastrointestinal Bleeding = any bleeding that starts in the gastrointestinal tract
o Symptoms can occur w/o warning, be sudden & severe or have a slow onset

o Acute GI bleeding can be life threatening if the cause of bleeding can’t be treated/controlled

 Common reason for a patient to be admitted to the ICU

 74-100% of critically ill patients develop stress-related GI mucosal erosions w/in 24H of admission that can lead to
serious GI bleeding

 Bleeding may come from any site along the GI tract, but is often divided into:
o Upper GI bleeding: The upper GI tract includes the esophagus (the tube from mouth to stomach), stomach, and first
part of small intestine

 Medical emergency associated w/ morbidity, mortality, & costly care

 4x more common than lower GI bleeding

 Commonly has s/s of hypovolemic shock

o Lower GI bleeding: The lower GI tract includes much of the small intestine, large intestine or bowels, rectum, and anus

 Has a lower morbidity & mortality

 Bleeding resolves spontaneously in the vast majority of patients

Distinguishing upper & lower GI bleeding by origin is an impt consideration - A rapid upper GI bleed may
present as a presence of blood in the lower GI tract
CLINICAL PRESENTATION
o Hematemesis
 Bright red bloody vomitus
Associated w/ fresh bleeding indicating upper GI bleeding

 Coffee-ground emesis
Caused when blood is mixed w/ digestive juices
Usually indicates that the bleeding has slowed/stopped

o Melena
 Black, tarry stool w/ a characteristic foul order
 Usually indicates upper GI bleeding sources (Because blood has gone through the GI tract)
o Hematochezia
 Fresh, red maroon stools
 Regardless of source, lower GI bleeding typically presents as this
But it can also occur w/ massive upper GI bleeding w/c is usually associated w/ orthostatic hypotension but most of
the time, it’s usually a lower GI bleeding source
CLINICAL PRESENTATION
o Syncope o Dyspepsia (indigestion)
o Epigastric pain
o Heartburn
o Diffuse abdominal pain
o Dysphagia
o Weight loss
o Signs of shock: hypotension, decreased pulses, decreased urine output
o Jaundice
TAKE NOTE:
DIAGNOSTICS
o Endoscopy = considered “gold standard” for diagnosis of GI bleeding
o Provides direct visualization of GI tract & bleeding site
o EGD
o Colonoscopy
o Radiographic procedures
o Upper & lower GI studies
o Serum blood studies
o CBC, metabolic profiles, coagulation profiles
TREATMENT
Fundamental goal of initial treatment: securing airway & initiating volume resuscitation Focus:
hemodynamic stabilization, identification of bleeding
Endoscopy w/in 12-24 H of admission is essential for those unstable upon admission or those who
continue to actively bleed after resuscitation

o Fluid resuscitation
 Adequate resuscitation and stabilization is essential
 Patients with active bleeding should receive IVF (e.g 500 mL of NS or RL over 30
minutes) while being crossmatched for blood transfusion
 Blood transfusion
 Must be individualized
 Approach is to initiate blood transfusion if hemoglobin is < 7 g/dL
(70g/L)
TREATMENT
o Hemostasis
 GI bleeding stops spontaneously in abt 80% of pxs
 Remaining pxs require some type of interventions
 Early intervention to control bleeding is important to minimize mortality, particularly
in elderly patients
o Airway
 Major cause of morbidity & mortality in pxs w/ active upper GI bleeding is aspiration of
blood w/ subsequent compromise
 To prevent these probs, endotracheal intubation should be considered in patients who
have inadequate gag reflexes or are obtunded or unconscious— particularly if they will be
undergoing upper endoscopy
o Active variceal bleeding
 Can be treated with endoscopic banding, injection sclerotherapy, or transjugular
intrahepatic portosystemic shunting (TIPS) procedure
TREATMENT
o General Support
 Supplemental oxygen via nasal cannula
 NPO
 Shock & bleeding must be controlled before oral intake
 Client should receive nothing by mouth during acute phase of GI bleeding
 When bleeding is controlled, diet can gradually be increased starting w/ ice
chips & then clear liquids
 PIVC (16G/18G) or a central venous line should be inserted
 Placement of a pulmonary artery catheter
 Elective endotracheal intubation
NURSING o All critically ill patients should be considered
at risk for stress ulcers and therefore GI
MANAGEMENT hemorrhage. Maintaining gastric fluid pH 3.5-
4.5 is a goal of prophylactic therapy
o Major nursing interventions are:
 Administering volume
replacement
 Controlling bleeding
 Maintaining surveillance for
complications (i.e. hemorrhagic shock)
 Educating family and patient
Intra-abdominal Hypertension and Abdominal
Compartment Syndrome
 Intra-abdominal Pressure = pressure concealed within the abdominal cavity
 Intra-abdominal Hypertension (IAH)
o Sustained pathological elevation of IAP greater than or equal to 12 mmHg
 Grade I: IAP between 12 - 15 mmHg
 Grade II: IAP between 16 - 20 mmHg
 Grade III: IAP between 21 - 25 mmHg
 Grade IV: IAP > 25 mmHg
o If untreated, IAH can lead to abdominal compartment syndrome
 Medical emergency that accts for significant morbidity & mortality in critically ill
patients
Intra-abdominal Hypertension and Abdominal
Compartment Syndrome
 Abdominal Compartment Syndrome (ACS)
o Organ dysfunction caused by intra-abdominal pressure > 20 mmHg– This is a medical
emergency!
o End-stage complication of untreated IAH
o Affects mesenteric, hepatic, & intestinal systems & can diminish blood flow to
intraabdominal organs
 Prevalence:
o IAH and ACS are not only related to trauma
 IAH and ACS are equally prevalent in medical patients
 Can be found in every critical care population
PATHOPHYSIOLOGY
o Initial injury (caused by trauma, hemorrhage, sepsis, hypotension, etc)---produces hypoxia of
intestinal tissues--- results in mild systemic inflammatory response (3 sequelae which develops
positive feedback loop: (1) release of cytokines, (2) oxygen free radicals produced, and (3) decreased
production of adenosine triphosphate (ATP); translocation of bacteria from gut to mesenteric lymph
nodes)
o Any secondary injury causes an exaggerated systemic inflammatory response
 Possibly caused by bacterial translocation additional release of cytokines perpetuates the
positive feedback loop
o Combination results in increasing IAP and hypoxia

Intra-abdominal Pressure Monitoring = the gold standard for diagnosing intra-abdominal

hypertension.
TREATMENT
o Titrate therapies for IAP lesser than or equal to 15mmHg
o Optimize fluid status
o Optimize systemic perfusion 
Goal abdominal perfusion pressure (APP) of greater than or equal to 60mmHg  APP = MAP – IAP
o Mean arterial pressure o Intra-abdominal pressure
o Evacuate intraintestinal contents
o Evacuate intra-abdominal lesions
o Improve abdominal wall compliance
o Consider emergent abdominal decompression
 Percutaneous drain to remove fluid
 Decompressive Celiotomy
 Bedside laparotomy
ACUTE PANCREATITIS
 Occurs suddenly as 1 attack or can be recurrent with resolutions; can be a medical emergency
 Due to self-digestion of pancreas by its own proteolytic enzymes
o Trypsin
 Other common causes aside from auto-digestion:
o Alcoholism: one of the most common cause
o Drug toxicity
o Abdominal trauma
o Biliary duct obstruction
ASSESSMENT
o Acute steady & severe epigastric pain that occur in the umbilical area and may radiate into the back. It is associated
with ingestion of alcohol or a fatty meal (cardinal sign)

 Pain is usually the main symptoms in pancreatitis and is aggravated when lying down

o N/V worsen with oral intake and does not relieve the pain

 Caused by the hypermotility or paralytic ileus secondary to pancreatitis or peritonitis

o Vital signs: fever, hypotension, tachycardia

o Abdominal rigidity, tenderness, distention, and decreased bowel sounds

o Grey Turner’s sign = reddish-brown to bluish discoloration along the flanks and represents accumulation of blood in the
area; a sign of severe necrotizing pancreatitis

 Death of pancreatic tissue causes bleeding into the abdomen

o Cullen’s sign = bluish discoloration around the umbilicus; also a sign of severe necrotizing pancreatitis

o Steatorrhea = fat content increases in volume as pancreatic insufficiency worsens  Bulky, fatty, foul-smelling stool
DIAGNOSTIC EVALUATION
o Increase serum lipase, amylase levels

 Used in making dx for acute pancreatitis

 Although in most cases, both are elevated w/in 24H of the onset of symptoms

 A: usually returns to n° in 48-72 hrs

SL: Remain elevated for a longer period, often days longer than amylase

o Increase urine amylase

o Leukocytosis or elevated WBC

o Hyperglycemia

 Important to closely monitor blood glucose levels in patients w/ pancreatitis because of the malfunction in the insulin
production

o Hypocalcemia

 If calcium is sequestered by fat necrosis

o Increase C-reactive protein

o Increase bilirubin and liver function test (indicates hepatic involvement)

o Imaging studies (e.g. Abdominal X-ray, UTZ, Ct-scan )

MEDICAL THERAPY
*directed towards relieving symptoms & preventing/treating complications
o Narcotic analgesics:

 Drug of choice: meperidine (Demerol)

 Med of choice to treat pain

 Morphine sulfate can cause spasms in the sphincter of Oddi thereby increasing bowel obstruction & exacerbating the
condition

o Antiemetics, antispasmodics and anticholinergics

 Decrease vagal stimulation, pancreatic secretion, & ampullary spasm

o Somatostatin = a treatment for acute pancreatitis, inhibits the release of pancreatic enzymes; known to inhibit GI, endocrine, exocrine,
pancreatic, and pituitary secretions, as well as modify neurotransmission and memory formation in the CNS

o Fluid resuscitation and electrolyte replacement

 Maintain circulatory volume & provide emergency treatment for shock

o Insulin administration as prescribed due to malfunction of insulin production

o Antibiotics
THERAPEUTIC AND SURGICAL MANAGEMENT
o NPO with NGT
 All oral intake is withheld to prevent stimulation of pancreas & secretion of enzymes
o IV and total parenteral nutrition
 Hypovolemic shock from fluid shift: major factor in acute pancreatitis
 Early fluid therapy is a cornerstone of treatment & is universally recommended for patients
w/ acute pancreatitis
o Peritoneal lavage
o Cholecystectomy after acute pancreatitis is resolved
NURSING MANAGEMENT
o Administer pain management as ordered

o Keep NPO with gastric suction

 Nasogastric suction is an option for pxs w/ consistent vomiting, gastric distention, ileus

 Reduces stimulation of pancreatic secretions by decreasing the contents that enters the small intestine

 Usually NG intubation w/ low intermittent suction

o Monitor lab results, v/s, intake/output bowel sounds

 Acute pancreatitis can cause decrease urine output w/c results from the renal failure that sometimes
accompanies this condition

o Maintain bed rest and may increase activity as tolerated

 Bed rest: to decrease metabolic rate & reduce secretion of pancreatic & gastric enzymes

o Place patient in a knee-chest position to facilitate relief of pain to reduce abdominal pressure & tension providing
some measure of comfort & pain relief

o Oral feeding is resumed when amylase levels return to normal and when pain is relieved o Small frequent, low fat,
feedings with no alcohol after acute phase

 Px w/ pancreatitis should avoid high fat food & alcohol

LIVER FAILURE
 Liver: largest organ of the body
o Essential role in regulating body’s metabolism
 An uncommon condition in which rapid deterioration of liver function results in coagulopathy and
alteration in mental status
o Common adverse complication: hepatic encephalopathy
 Liver failure indicates that liver has sustained injury
 Types of Liver Failure:
o Fulminant Hepatic failure = encephalopathy starts within 8 weeks
 Otherwise known as acute failure
 Results in a rapid deterioration of liver fxn in a person w/o prior liver dse
 Cellular insult results in a massive cell necrosis leading to multiple organ dysfxn
o Non fulminant hepatic failure = encephalopathy starts between 8-26 weeks
LIVER FAILURE
 Acute Liver Failure
o Is a rare condition characterized by the abrupt onset of severe liver injury
o Loss of liver function that occurs rapidly – in days or weeks – usually in a person who has no pre-
existing liver disease o It’s a medical emergency that requires hospitalization
o Leading cause: Acetaminophen overdose
o Other causes: Viral hepatitis (A, B, E)  Thrombosis  Shock
o Patient history:
 Focus: exposure to viral infxns, drugs or other toxins or other receninjuries/illnesses

 Patient & family should be questioned abt acetaminophen intake

 Acetaminophen toxicity

o Antidote:

 N-acetylcysteine (NAC or Mucomyst) Activated charcoal  Decontamination agent

 Prevents absorption of acetaminophen by absorbing drug in the intestine

LIVER FAILURE
o Clinical Manifestation:
 Jaundice
 2ndary to excessive deposition of bilirubin in skin tissues, mucousmembrane, sclera
o Represents failure of liver to adequately uptake, conjugate & excrete bilirubin

o Bec of this, jaundice is typically evident when bilirubin exceeds 2-3 mg/dL

 Hepatic encephalopathy (mental confusion, difficulty concentrating and disorientation)

o Altered mental status & level of consciousness

o Neurological status requires vigilant assessment because hepatic encephalopathy, cerebral edema, & increased ICP can rapidly progress
into brain & death)

 Pain and tenderness in the upper right side of the stomach

 Electrolyte imbalances (hypoglycemia, hypokalemia, hypomagnesemia, hypocalcemia, and
hypophosphatemia)
o Hypoglycemia develops due to massive hepatic cell necrosisthus there will be a diminished glucose release

o Hypokalemia may occur from inadequate oral intake potassium loss from vomiting
LIVER FAILURE
o Clinical Manifestation:
 Melena
 Ascites
o Accumulation of fluid in the stomach due to a lot of factors
 Portal hypotension, hypoalbuminemia, inactivation ofRAA mechanism (aldosterone-antidiuretic hormone)thereby promoting fluid
retention in the body

 Ankle edema
o Albumin is responsible for maintaining colloid osmotic pressure in the vascular system

o In the absence of albumin, fluids from the vascular system could cross over into the interstitial space thus the accumulation of fluid in
the legs, ankle, & feet

 Malaise, drowsiness, and muscle tremors

 Bleeding, cerebral edema, hematemesis, coma
o Bleeding: Increased PT or INR > 1.5
LIVER FAILURE
o Management:
 Treatment of acute liver failure consists of drugs and liver transplantation

 Pharmacological management includes certain antidotes to reverse the effects of ALF and various medication to reduce
ICP

 Penicillin G, activated charcoal, N-acetylcysteine, osmotic diuretics(mannitol to decrease cerebral edema), barbiturate
(phenobarbital when severe intracranial hypertension doesn’t respond to any measures), benzodiazepine, and anesthetic
agents (propofol –sedative hypnotic to reduce cerebral blood flow)

 Nursing Interventions:

 Assess, report, and record signs and symptoms and reactions to treatment

 Monitor fluids input and output closely

 Observe for signs of dehydration, 2ndary infection, neurologic disturbances, edema, jaundice

 Provide adequate diet with high proteins, CHO, and vitamins (carefully monitor this in encephalopathy)

 Monitor for signs of possible bleeding

LIVER FAILURE
o Management:
 Other interventions:

 For coagulopathy/GIT bleeding – vitamin K can be given to treat abnormal PT

 Correction is needed prior to undergoing invasive procedures

 Hypotension should be treated with fluids

 Pulmonary complications – mechanical ventilation may berequired esp for mgmt. of cerebral edema & acute respiratory
distress syndrome

 Head of bed should be elevated to 30 degree

 Monitor neurologic status

o Hepatic encephalopathy is a major complication of ALF & a prognostic marker bec it is progressive unless LF is resolved

o Goal is to maintain intracranial pressure below 20 mmHg, andcerebral perfusion pressure above 50-60 mmHg

o Judicious administration of sedation and analgesia for patientsexperiencing agitation during certain stages of Hepatic
encephalopathy.

 Treatment would focus on resolution of LF, decreasing ammonia lvl, & monitoring ICP w/ interventions to decrease cerebral
edema
HYPERGLYCEMIA
o During acute illness, liver produces & releases glucose in response to glucocorticoids,
catecholamines, growth hormones, etc.
o As a result of this, fat & proteins are catabolized & blood sugar surges
o Conditions such as MI, stroke, surgery, trauma, pain may cause release of these biological mediators
& counter regulatory hormones
o The greater the stress response, the higher the blood pressure
 Rigorous glucose monitoring & effective mgmt. of blood glucose are essential
o Usually accomplished in critically ill patients by frequent blood glucose monitoring paired w/
continuous insulin infusion
 Medical term describing an abnormally high blood glucose level
 Hallmark sign of diabetes (both type 1 and type 2 DM)
HYPERGLYCEMIA
 Signs and symptoms:
o 3 Ps: Polyuria, Polydipsia, Polyphagia
o Viscous blood w/c could lead to poor circulation
o Altered sensation
o Glycosuria due to damaged glomeruli
o Diabetic foot w/c could be a complication of hyperglycemia/diabetes
o Risk for infection and dehydration
o Hot and dry skin
o Hypertension (with headache)
o Fatigue, blurred vision, slurring of speech
HYPERGLYCEMIA
 Precautionary measures:
o Follow diabetes meal plan, exercise program, and medication routine
o If blood sugar levels are above target range, drink extra liquids
 Helps replace fluids lost through urine
 Water & sugar-free drinks are best
 Drink non-caffeinated & non-alcoholic beverages that do not contain sugar
 Instruct patient to avoid drinks w/ a lot of sugar (fruit juice)
o Monitor blood sugar often
o Normal blood glucose ranges from 70 to 110 mg/dL
HYPERGLYCEMIA
 Treatment:
o Control of high glucose level:
 Raise insulin dose as prescribed & titrate thereafter
 Recommend dietary changes
 Recommend more exercise (at least three times a week to meet goals of planned exercise, thereby
lowering blood glucose levels, reducing/maintaining proper weight)
 Recommend closer glucose monitoring
DIABETIC KETOACIDOSIS
 A life-threatening complication of DM that develops when severe insulin deficiency occurs
 Main clinical manifestations:
o Hyperglycemia, dehydration and electrolyte loss due to polyuria, and acidosis
o During acute illness, things such as breakdown of fat increases due to increased metabolic demands,
thereby increasing ketones. That is why there is a presence of acidosis in DKA
 More common to occurs in patients with Type 1 DM
 Causes:
o Decreased or missed dose of insulin
o Illness or infection
 Release of cortisol due to stress decreases production of insulin. Thus, increasing risk of DKA
DIABETIC KETOACIDOSIS
 Assessment:
o Elevated blood glucose level 300-800 mg/dL
o Decreased serum bicarbonate and pH
o Sodium and potassium may be low
o Glycosuria; polyuria; dehydration
o Metabolic acidosis
 As a compensation, patient will exhibit Kussmaul’s respiration/breathing
 Deep, labored, fast breathing

 Happens when body tries to remove Co2 & acid from the body by quickly breathing it out

 Compensatory mechanism of the body to correct acidosis

o Sweet breath odor

 Due to high levels of ketones
DIABETIC KETOACIDOSIS
 Indications WHEN to contact a medical practitioner
o Decreased consciousness o Difficulty breathing o Fruity breath
 Implementation:
o Restore circulating blood volume
o Treat dehydration with rapid IV infusions
 e.g bolus PNSS/.9 NACL to promote circulation and dilute sugar

o Treat hyperglycemia with IV regular insulin

 Usually, IV bolus is done for correction first then continuous infusion thereafter to titrate it depending on the px’s blood
glucose levels

o Cardiac monitoring & electrolyte replacement

o Treat acidosis according to cause (check ABG)
 Give antacids: Sodium bicarbonate to correct acidosis
DIABETIC KETOACIDOSIS
 Prevention:
o Restore circulating blood volume
o Educate patients in recognizing early S/S of DKA
o Emphasize not to eliminate insulin doses when nausea and vomiting occur
o Should have available foods for use on a “sick day”
o Drink fluids every hour to prevent dehydration
o In people with infections or who are on insulin pump therapy, measuring urine ketones can give more
information than glucose measurements alone
 Ex. Spot test
o Measures ketones in urine
o Kit contains dipsticks coated w/ chemicals that react w/ ketone bodies
o Dipstick is dipped in urine sample & a color change would indicate presence of
ketones
HYPERGLYCEMIC-HYPEROSMOLAR
NONKETOTIC SYNDROME (HHNS/HONKS)
 Also known as “Hyperosmolar hyperglycemic state”
 Extreme hyperglycemia without ketosis and acidosis
 Characterized by hyperglycemia, hyperosmolarity, & dehydration w/o ketosis
 Occurs in patients with Type 2 DM
o DKA: Type 1
 Onset is usually slow and takes hours or days to develop
 Causes:
o Leading cause: Inadequate fluid replacement o Insufficient insulin o Major stresses
HYPERGLYCEMIC-HYPEROSMOLAR
NONKETOTIC SYNDROME (HHNS/HONKS)
 Assessment:
o Blood glucose is from 600 - 1200 mg/dL
o Hypotension o Dehydration
o Tachycardia
o Mental status changes and neurological deficits
o Seizures
o Polydipsia (special craving for cold water), polyuria, increased plasma osmolality (>320mosm/kg)
[NV: 275-295 mOsm/kg], high urine specific gravity (>1.010)
 Higher urine specific gravity = higher risk for dehydration
HYPERGLYCEMIC-HYPEROSMOLAR
NONKETOTIC SYNDROME (HHNS/HONKS)
 Assessment:
o Blood glucose is from 600 - 1200 mg/dL
o Hypotension o Dehydration
o Tachycardia
o Mental status changes and neurological deficits
o Seizures
o Polydipsia (special craving for cold water), polyuria, increased plasma osmolality (>320mosm/kg)
[NV: 275-295 mOsm/kg], high urine specific gravity (>1.010)
 Higher urine specific gravity = higher risk for dehydration
HYPERGLYCEMIC-
HYPEROSMOLAR
NONKETOTIC SYNDROME
(HHNS/HONKS)

 Implementation:
o Similar treatment with DKA
o Includes fluid replacement, correction of
electrolyte imbalances
o Hypokalemia
 Administer KCL & insulin
administration
HYPERGLYCEMIC-HYPEROSMOLAR
NONKETOTIC SYNDROME (HHNS/HONKS)
 Assessment:
o Blood glucose is from 600 - 1200 mg/dL
o Hypotension o Dehydration
o Tachycardia
o Mental status changes and neurological deficits
o Seizures
o Polydipsia (special craving for cold water), polyuria, increased plasma osmolality (>320mosm/kg)
[NV: 275-295 mOsm/kg], high urine specific gravity (>1.010)
 Higher urine specific gravity = higher risk for dehydration