ACUTE GASTROINTESTINAL HEMORRHAGE
GI hemorrhage is a potentially life-threatening emergency and a
common complication of critical illness, occurring from bleeding
in the upper or lower GI tract.
CAUSES
PROXIMAL (Upper GI
Tract)
Esophagastric Varices
Stress-Related Mucosal
Disease (SRMD)
D
E
ALTEROLIC,
A
N L,
M
B
E
A
T
N
I
T
GA
ES O
S T R O I N T E TI
C
AND
N
U
LIV E R F
BSN 4C | GROUP 3
BOLORON | BUREROS | ESPLANADA | GUISANDO | MAQUILAN | NOB | SANDIG
Peptic Ulcer Disease
HALLMARK SIGNS
AND SYMPTOMS
Hematemesis
Hypotension
DISTAL (Lower GI Tract)
Diverticulosis
Hemorrhoids
GOLD STANDARD
DIAGNOSTICS
ENDOSCOPY - To
Localize and treat
bleeding source.
Melena
Hematochezia
Abdominal Pain
Oliguria/Anuria
MANAGEMENT
Fluid Resuscitation; IV
Stress
Crystalloids,
Techniques;
blood
Reduction
Guided
products.
Imagery,
Vasopressin infusion .
Techniques .
Surgery; Vagotomy +
Initially
Pyloroplasty,
bleeding is controlled
Shunt
Avoid
Procedures.
Pharmacology;
PPI,
H2 Blockers, Antacids.
Breathing
NPO
until
alcohol,
caffeine, spicy foods,
NSAIDS.
NURSING DIAGNOSES
Deficient Fluid Volume related to acute blood loss
Decreased Cardiac Output related to altered preload
and hypovolemia
INTRA-ABDOMINAL HYPERTENSION AND
ABDOMINAL COMPARTMENT SYNDROME
ACUTE LIVER FAILURE
IAH is a sustained increase in pressure within the abdominal
cavity (≥12 mmHg).
It can reduce blood flow to vital organs, leading to
complications.
ACS occurs when abdominal pressure rises to dangerous
levels (≥20 mmHg with organ dysfunction).
CAUSES: “3 F’S ”
Fluid overload
–massive IV fluids, ascites,
bleeding
Full belly
–abdominal
trauma,
tumors,
tight
dressings/surgery
Failure of organs
–sepsis,
pancreatitis,
obstruction
HALLMARK SIGNS
AND SYMPTOMS
Progressive abdominal
distension
(tense, firm belly)
Oliguria/Anuria (↓ urine
output)
CAUSES
PATHOPHYSIOLOGY
RUGS/TOXINS
In acute liver failure, massive hepatocyte injury from
toxins, viruses, ischemia, or metabolic disorders
overwhelms the liver’s ability to regenerate. This leads to
impaired detoxification, causing ammonia buildup and
cerebral edema (encephalopathy). Loss of gluconeogenesis
and glycogen stores results in hypoglycemia, while reduced
synthesis of clotting factors and albumin causes
coagulopathy, ascites, and edema. Failure to clear bilirubin
produces jaundice, and impaired immune protein synthesis
increases infection risk. As the injury progresses, multiorgan complications such as renal failure, acidosis,
cardiovascular collapse, and ARDS may develop, with liver
transplant as the only definitive cure.
IRAL
MMUNE
Gold Standard Diagnostics
REGNANCY
Bladder pressure measurement
via Foley catheter
ETABOLIC
NEMIA/ISCHEMIA
OST-OP/TRANSPLANT
IAH grade I (12-15 mm Hg)
IAH grade II (16-20 mm Hg)
IAH grade III (21-25 mm Hg)
IAH grade IV (greater than 25 mm Hg)
YNDROMES
HALLMARK SIGNS AND SYMPTOMS
NURSING DIAGNOSIS
Excess fluid volume related to fluid
accumulation in the abdominal cavity.
Ineffective breathing pattern related to
diaphragmatic elevation and
lung
compliance.
Risk for impaired renal perfusion related to
increased intra-abdominal pressure.
↓
MANAGEMENT
Medical: Optimize fluid balance,
diuretics, drain ascites/collections,
improve ventilation
Surgical: Decompressive
laparotomy (if ACS develops)
↑ Intra-abdominal pressure
(measured via bladder
pressure)
A life-threatening condition characterized by severe and sudden
liver cell dysfunction, coagulopathy, and hepatic encephalopathy
(Urden et al., 2022).
Diuretics
(Furosemide):
Vasopressors
(Norepinephrine):
Sedatives/Analgesi
cs ↓ abdominal
wall tension
Nursing:
Monitor IAP and urine output closely
Elevate head of bed ≤20–30° (avoid excessive
abdominal pressure)
Strict fluid balance and daily weights
Provide oxygen/ventilatory support as needed
Hepatic Encephalopathy
Coagulopathy
Jaundice
Gold Standard Diagnostics
INR ≥1.5 + Hepatic Encephalopathy (no
RUQ Pain
NURSING DIAGNOSIS
prior liver disease, onset <26 wks).
SAVE LIVER
Hypoglycemia
Impaired Gas Exchange
Acute Confusion
Risk for Bleeding
MANAGEMENT
Supportive ICU care
Electrolytes & Glucose
correction
Antidote: Nacetylcysteine (NAC)
FIRST-LINE
Lactulose ± rifaximin
Vasopressors/fluids
Infection control
Vitamin K / blood
products
Early
transplant
referral
DEFINITIVE TX.
RRT (CRRT)
ACUTE PANCREATITIS
Acute pancreatitis is an inflammation of the pancreas that
produces exocrine and endocrine dysfunction that may also involve
surrounding tissues, remote organ systems, or both.
CAUSES: “ I GET SMASHED”
Steroids
Idiopathic
Mumps
Gallstones
Autoimmune
Ethanol
Scorpion Sting
Trauma
Hyperlipidemia
ERCP (Endoscopic Retrograde
Cholangiopancreatography)
PATHOPHYSIOLOGY
Acute pancreatitis occurs when triggers such as gallstones,
alcohol, trauma, or drugs cause ductal obstruction or acinar
cell injury, leading to premature activation of trypsinogen to
trypsin and subsequent autodigestion of pancreatic tissue.
Activated enzymes like elastase and phospholipase cause
acinar damage, fat necrosis, vascular injury, and local
inflammation, while cytokines such as TNF-α, IL-1, and IL-6
amplify edema, necrosis, and hemorrhage. In severe cases,
these mediators enter the circulation, triggering systemic
inflammatory response syndrome (SIRS) that can progress to
ARDS, shock, renal failure, and multi-organ dysfunction.
Drugs
GOLDEN STANDARD
DIAGNOSTICS
HALLMARK SIGNS & SYMPTOMS
“PLA-C”
Pain (acute epigastric pain radiating
to the back)
Lipase (gold standard lab test, ≥3×
normal)
Severe Epigastric
Pain
Nausea & Vomiting
Cullen’s Sign
Amylase (also elevated, but less
specific)
C – Contrast-enhanced CT (gold standard
imaging, for severity/complications)
MANAGEMENT
NPO & IV fluids – bowel rest with
aggressive hydration.
Pain control – opioids for analgesia.
Oxygen & electrolytes – maintain
oxygenation, correct imbalances.
Nutrition – early oral intake if mild; enteral
feeding if severe.
Treat cause – ERCP/cholecystectomy
(gallstones), stop alcohol/drugs, treat
hypertriglyceridemia.
Complications – antibiotics + drainage for
infected
necrosis/abscess;
manage
pseudocysts if large or symptomatic.
Core idea: Rest, Resuscitate, Relieve pain,
Remove cause, and Manage complications.
👉
Abdominal
Tenderness
& Distention
Fever,
Tachycardia
& hypotension
Grey Turners Sign
NURSING DIAGNOSIS
1. Acute Pain related to inflammation and enzymatic autodigestion of pancreatic
tissue as evidenced by severe epigastric pain radiating to the back, abdominal
tenderness, and guarding.
2. Deficient Fluid Volume related to fluid shifting into the retroperitoneal and
peritoneal spaces (third spacing) as evidenced by hypotension, tachycardia, dry
mucous membranes, and decreased urine output.
3. Imbalanced Nutrition: Less Than Body Requirements related to impaired
digestion and absorption secondary to pancreatic inflammation as evidenced by
anorexia, nausea, vomiting, and weight loss.
4. Risk for Infection related to necrotic pancreatic tissue and potential translocation
of bacteria.
5. Ineffective Breathing Pattern related to diaphragmatic splinting and reduced lung
expansion secondary to abdominal pain and distention as evidenced by tachypnea,
dyspnea, shallow respirations, and decreased oxygen saturation.
DIABETIC KETOACIDOSIS
is an acute, life-threatening complication of diabetes,
characterized by the triad of hyperglycemia, ketosis, and
metabolic acidosis resulting from insulin deficiency and
increased counterregulatory hormones.
CAUSES: 4S
SEPSIS
SICKNESS “STOMACH
VIRUS AND FLU”
STRESS (SURGERY)
SKIP INSULIN
Gold Standard
Diagnostics
REMEMBER “ABC-K”
Acidosis (pH < 7.3, HCO₃ < 18)
Blood glucose > 250 mg/dL
Circulating ketones
(ketonemia/ketonuria)
Ketone measurement (βhydroxybutyrate = best test)
NURSING
DIAGNOSIS
Deficient Fluid Volume related to
osmotic diuresis and dehydration.
Decreased Cardiac Output related to
alterations in preload.
Risk for Electrolyte Imbalance related
to osmotic diuresis and insulin
therapy.
Anxiety related to threat to biologic,
psychologic, and social integrity.
Ineffective
Coping
related
to
situational crisis and personal
vulnerability.
Disturbed Body Image related to
functional dependence on lifesustaining technology (IV insulin,
monitoring).
PATHOPHYSIOLOGY
In diabetic ketoacidosis, a lack of insulin prevents glucose from
entering cells, leaving them starved of energy while blood
glucose levels rise. The kidneys attempt to remove the excess
glucose, causing osmotic diuresis that leads to polyuria,
dehydration, and electrolyte loss. To compensate for the lack of
glucose inside cells, the body breaks down fat into free fatty
acids, which are converted into ketones. The buildup of ketones
causes metabolic acidosis, leading to Kussmaul respirations and
fruity acetone breath. Together, hyperglycemia, dehydration,
electrolyte imbalance, and acidosis form a vicious cycle that
defines DKA.
HALLMARK SIGNS AND SYMPTOMS
Polyuria
Polydipsia
Fruity acetone
breath odor
Dehydration
Kussmaul
respirations
Altered
mental status
MANAGEMENT
REMEMBER FIRE
F – Fluids: IV normal saline (0.9% NaCl), then adjust
(0.45% NaCl or D5W once glucose <200 mg/dL).
I – Insulin: IV regular insulin infusion (0.1 u/kg/hr).
Continue until acidosis resolves.
R – Replace Electrolytes: Especially potassium
(replace if <5.3 mEq/L and patient urinating);
phosphate if <1 mg/dL.
E – Evaluate Acidosis: Monitor ABGs; give
bicarbonate only if pH < 7.0.
COMPARATIVE TABLE
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