Chem- to check electolytes

BUN- will ↑ with bowl obstruction or blood loss of > 2 units

Lactic acid- ↑ if bowl infarcted and metabolic acidosis

APL- ↑ intestenal and hepatic injury

Amylase-↑ ulcers or intestinal obstuction

What Diagnostic Tests would be done on your pt with abd pain

X-ray- free air = bowl perf, asol see obstuctions

CT- masses abcess

MRI- masses abcess

Ultrasound- shows liquids or solid masses

Endoscopy- see physical structures 

#1 peptic ulcer disease

other causes: Gastritis

Mallory-Weiss tears

Varices

Mallory-Weiss syndrome is characterized by upper gastrointestinal bleeding secondary to longitudinal mucosal lacerations (known as Mallory-Weiss tears) at the gastroesophageal junction or gastric cardia. 

 Mallory-Weiss syndrome may occur after any event that provokes a sudden rise in intragastric pressure or gastric prolapse into the esophagus (persistent retching and vomiting following an alcoholic binge)

You pt has an upper GI bleed you know this means the bleed is:

A. arterial and slow

B. venous and fast

C. venous and slow

D. arterial and fast

You will see BRB in the stool and vomit of a pt with a upper GI bleed.

True or False?

True

The pt is bleeding so fast and so much that the blood does not have time to break down 

Diverticuli

Ischemic bowel

Inflammatory bowel disease

Neoplasms

You pt has an lower GI bleed you know this means the bleed is:

A. arterial and slow

B. venous and fast

C. venous and slow

D. arterial and fast

Altered level of consciousness

 Decreased urine output

 Hypotension

 hematemesis- vomiting blood

melena- black stools

hematochezia- BRB in stool

Your pt has a GI bleed and a ↓ LOC, what is your best nursing action to keep this pt safe?

Why?

place artificial airway.

Pt is at high risk of aspirating blood  from vomit.

Your pt has a upper GI bleed and need RBC's.

What needs to be done before giving the blood?

restore intervasculer vol. first 1-3L of cristalloids (NS),

then the pt may recive the blood. 

The  BP is maintained at SBP > 90

 and the Hct >28-30

The HCT ( 36-72 hrs) can be concentated or diluted do you also want to see trends in the right diretion. 

Eppi- helps controles the bleeding 

carafate- adheres to damaged ulcer tissue and protects against acid and enzymes so healing can occur.

Cautery

 Clipping

inject eppi

Sengstaken-Blakemore tube

What is a Levophed lavage

levophed is used in an upper GI bleed to stop the bleeding it goes in by NG washes over the bleeds and is pulled back out. 

***Must get same amount back out

What is the hallmark sign of Acute Bowel Obstruction

abdominal distention. 

Rebound tenderness may occur with perforation.

Extracellular fluid is drawn into bowel lumen, fluids and elctrolytes third space into the peritoneum leading to hypotension.

mild/steady pain, vomiting is uncommon, pronounced distention, no BM

“crampy” pain in waves, bilious vomiting, dehydration, “tinkling” bowel sounds, mild distention, BM till clear

WBC- mild increase

NA- ↑

BUN-↑

Creat-↑

Serum osmo- ↑

NPO

NG to suction

Fluid replacement

Laxatives

Enemas

Surgery- if hopotensive

Colostomy/Ileostomy

What Conditions are associated with intra-abdominal hypertension and abdominal compartment syndrome

Sepsis / SIRS / Ischemia Reperfusion

Visceral compression / Reduction

Surgical procedures

Critical Obstetrical conditions

Trauma

Ischemia

Capillary leak 

What are the risk factors for Sepsis / SIRS / Ischemia Reperfusion  

·         Sepsis and resuscitation with > 5 liters fluid in 24 hours

·         Ongoing requirement of vasopressors to support tissue perfusion

·         Pancreatitis

·         Peritonitis, colitis

·         Ileus / Bowel obstruction

·         Mesenteric ischemia / necrosis 

Visceral compression / Reduction 

·         Large ascites/ peritoneal dialysis

·         Retroperitoneal / abdominal wall bleeding

·         Large Abdominal tumor

·         Laparotomy closed under tension

·         Gastroschisis / Omphalocele 

·         Intra-operative fluid balance > 6 liters

·         Abdominal aortic aneurysm repair 

Critical Obstetrical conditions 

·         Preeclampsia and eclampsia

·         Pregnancy related DIC 

·         Shock requiring resuscitation (ischemia-reperfusion)

·         Damage Control Laparotomy

·         Multiple trauma with or without abdominal trauma

·         Major burns (> 25%) 

Ischemia + Capillary leak

·         Systemic inflammatory response 

·         Fluid resuscitation

·         Intra-abdominal Hypertension

·         Tissue Edema (Including bowel wall and mesenteric edema) 

What are the S/S of increased abdominal pressures

Tense abdominal wall

Shallow respirations

Increased central venous pressure

Oliguria.

Elevated Intra-abdominal Pressures

How is  Intra-abdominal Pressures monitered?

Mild Abd Hypertension: 10 to 20 mmHg

Moderate Abd. Hypertension: 21 to 35 mmHg

Severe Abd. Hypertension: 35 mmHg 

Your pts IAP was at 5 and is now 10. What is the nurses best action.

A. Call the MD

B. continue to monitor this is not a significant rise

A. Call the MD

Early interventions are need to prevent ACS and MODS

damage is irreversible once IAP is 20

treatment for mod-severe IAP includes:

surgical decompression 

causes:

 Compression of the vena cava with reduction in venous return to the heart.

Decreased cardiac output leads to increased SVR

Increased cardiac workload

Decreased tissue perfusion

Misleading elevations of CVP and PAWP

Cardiac insufficiency leads to Cardiac arrest 

Elevated intra-abdominal pressure causes:  Compression of renal veins, parenchyma, Reduced cardiac output to kidneys

The Result:

     Reduced blood flow to kidney

Renal congestion and edema

Decreased glomerular filtration rate (GFR)

Renal failure, oliguria/anuria  

Increased intra-abdominal pressures causes: Compression / Congestion of mesenteric veins and capillaries (capillary flow 25 mm arterial down to 15 mm venous). Reduced cardiac output to the gut 

 The result:

 Decreased gut perfusion, increased gut edema and leak

Ischemia, necrosis, cytokine release, neutrophil priming

Bacterial translocation

Development and perpetuation of SIRS

Further increases in intra-abdominal pressure

Increases in intrathoracic pressure

Increases in superior vena cava (SVC) pressure with reduction in drainage of SVC into the thorax

 The Result:

 Increased central venous pressure and IJ pressure

Increased intracranial pressure      

Decreased cerebral perfusion pressure

Cerebral edema, brain anoxia, brain injury

Elevation of the diaphragms with reduction in lung volumes, stiffening of thoracic cage, reduced alveolar inflation, increased intersitial fluid (lymp obstruction)

 The result:

 Elevated intrathoracic pressure

Increased peak pressures, Reduced tidal volumes

interstitial edema, Atelectasis, hypoxia, hypercarbia

Ventilator Induced lung injury/Barotrauma

Cytokine release - pro-inflammatory response,   ARDS

What are the diffrent functions of the Liver 

Metabolic Functions

Blood reservoir, filter, aids clotting

Drug metabolism and detoxification

What might you asume if your pts labs are:

ALT+ AST > APL + GGT

What might you asume if your pts labs are:

APL+GGT > ALT + AST

What might you asume if your pts labs are:

ALT< 300 and AST:AST > 2:1

The liver takes the byproduct of RBC breakdown, bilirubin and conjugates it for excretion. When we see high level of unconjugated bilirubin or jaundice it indicates liver dysfunction.

Viral hepatitis

Toxins (all except ETOH)

Biliary disease

Viral  hepatitis

ETOH toxicity

Shock states/ MODS

weeks to months 

lasts until enzyms are normal

GI bleeding

Constipation

Azotemia ( Hepatorenal Failure)- high nitrogen levels

Increased protein intake

lactulose- ^ parastolsis

neomycin- binds to amonia

What is Portal Hypertension

Congestion of sinusoids decreases portal blood flow rate (normally 1.5 L/min) and increases pressure in the sinusoids (normally 2 - 7 mHg).

Hepatic pressure > 20 mmHg causes plasma to weep through to peritoneum and reflect high pressure back to gastric / mesenteric vasculature

What are the complictions of Portal Hypertension

Ascites

Varices

sepsis

Hepatorenal syndrome

What is Hepatorenal syndrome Type I 

Identify and treat precipitating factors

 Maintain normal ammonia levels

Maintain fluid / electrolyte balance

 Control bleeding

 Monitor renal function

 Drain ascites as needed for respiratory function

1. Biliary (more common in women)

2. Infection

3. Toxins:  ETOH (#1), Tetracycline, Sulfa, Thiazides, Methyldopa

Trypsin

Lipase

Elastase

activation of the clotting cascade, DIC

Vasodilation

Increased capillary permeability

distuction of cell membranes

damages sufactant

(Non-hemorrhagic)

Most common 95%

Low mortality

(Hemorrhagic)

> 50% mortality

Cullen’s sign

Grey-Turner sign

What is Cullen’s Sign

What does  Cullen’s Sign indicate 

Acute pancreatitis

Aortic aneurysm, abdominal

Blunt abdominal trauma

Ectopic pregnancy

Ruptured ectopic pregnancy 

What is Grey Turner Sign

is bruising of the flanks. It occurs in severe, acute pancreatitis due to subcutaneous tracking of inflammatory, peripancreatic exudate from the pancreatic area of the retroperitoneum.

Amylase- doesn’t indicate severity, can obtain Isoamylase

Lipase:  elevated the longest,

**opioids or food within 8 hours can cause false elevation

Bilirubin:  only increases if bile duct occlusion

Glucose:  only elevates if endocrine islets are affected

What is the Ranson Criteria

Predicts severity of Pancreatitis

If more than 3 criteria are present, admit to ICU

Assessment is done on admission and 48 hours later

What are the complications of pancreatits 

Shock- Hypovolemia due to vasodilation and capillary permeability or hemorrhage

Pseudocysts-  May contain enzymes, blood or necrotic tissue

Abscess- Related to an infectious process

Hemodynamics:  May require 10 - 20 L in the first 20 hours,  may require inotropes

Pain control:  Demerol or Dilaudid preferred

Pancreatic rest:  NPO until amylase is normal and patient is having no pain

Prevent / treat complications