5.2 Complications of Shock

Question 1

MODS (Multiple Organ Dysfunction Syndrome)

Answer 1

• Organ dysfunction in acutely ill patients where homeostasis cannot be maintained without intervention
• Most commonly occurs secondary to septic shock (but can also be trauma, neoplasia, or other causes of SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)
• It has degrees and is a process not a single event.

Question 2

MODS

Answer 2

• End result of shock and sepsis

Triggers
- Multiple injuries
- Burns
- Hemorrhagic/Hypovolemic Shock
- Acute Pancreatitis
- Acute Respiratory Distress Syndrome (ARDS)
- Acute Renal Failure
- Severe Sepsis also results in systemic inflammatory response

Question 3

Deitch Theory Gut Hypothesis

Answer 3

• Splanchnic (visceral) hypoperfusion causes structural and functional changes in cells. This results in gut permeability which causes translocation of bacteria. Liver Dysfunction leads to toxins that escape to systemic circulation activating the immune system which results in tissue injury and organ dysfunction

Question 4

MODS Criteria

Answer 4

• Presence of 2+ organ dysfunction in acutely ill patients requiring intervention
• Can be primary or secondary
• High mortality rate

Question 5

MODS Treatment

Answer 5

• Control initiating event
• Promoting adequate organ perfusion
• Provide adequate nutrition
• Promote communication

Question 6

Progression of MODS

Answer 6

• Inflammatory response leads to hypermetabolism and misdistribution of blood flow which causes perfusion issues and organ damage/cell death.

Question 7

Primary (Early) MODS

Answer 7

• Local and generalized hypoperfusion triggers inflammatory and stress responses

Question 8

Secondary (Late) MODS

Answer 8

• Excessive inflammatory response manifested in organs distant from original injury
• Activates inflammatory response, coagulation, and fibrinolysis

Question 9

Manifestations of MODS

Answer 9

• Respiratory failure within first 72 hours
• Liver failure 5-7 days after injury
• GI Bleed 10-15 days
• Renal failure 11-17 days

Question 10

Pulmonary Manifestations

Answer 10

• Dyspnea
• Refractory Hypoxemia
• Respiratory Acidosis
• Abnormal O2 Indices
• Patchy Infiltrates
• Pulmonary Hypertension

Question 11

GI Manifestations

Answer 11

• Mucosal Ulcerations
• Abdominal distension and ascites
• Bacterial overgrowth in stool
• GI BLEEDING
• Paralytic Ileus
• Intolerance of Enteral Feedings

Question 12

Liver

Answer 12

• Increased bilirubin, liver enzymes, serum ammonia
• Jaundice
• Hepatomegaly

Question 13

Cardiovascular (Hyperdynamic)

Answer 13

• Increased o2 consumption, cardiac output, cardiac index, heart rate
• Decreased pulmonary capillary wedge pressure (PCWP), SVR, right atrial pressure

Question 14

Cardiovascular (Hypodynamic)

Answer 14

• Increased SVR, right atrial pressure, left ventricular stroke work index

Decreased oxygen delivery/consumption, cardiac output, cardiac index

Question 15

Metabolic/Nutritional

Answer 15

• Muscle wasting, Weight loss, Decreased lean body mass
• Increased serum lactate
• Decreased serum albumin
• Hyperglycemia/Hypertriglyceridemia
• Negative nitrogen balance

Question 16

Renal

Answer 16

• Increased serum creatinine and BUN
• Oliguria/Anuria
• Possible polyuria
• Acute tubular necrosis

Question 17

CNS

Answer 17

• Lethargy/LOC
• Fever
• Hepatic Encephalopathy

Question 18

Coagulation/Hematologic

Answer 18

• Thrombocytopenia
• Disseminated Intravascular Coagulation (DIC)

Question 19

Immune

Answer 19

• Infection
• Decreased lymphocyte count
• Anergy (absence of normal immune response to specific antigens/allergens)

Question 20

ARDS (Acute Respiratory Distress Syndrome)

Answer 20

• RESPIRATORY SYSTEM IS THE FIRST TO FAIL

Question 21

Causes of Renal Failure

Answer 21

• Hypovolemia
• Hypotension
• Reduced CO and HF
• Obstruction of kidneys, lower urinary tract, renal arteries/veins
• Leads to increased creatinine and reduction of urine output
• Azotemia (increased BUN or creatinine in blood)

Question 22

Prerenal Causes

Answer 22

• Decreased perfusion and PVR
• Regulatory mechanisms attempt to preserve blood flow

CAUSES ARE EXTERNAL TO THE KIDNEYS THAT REDUCE RENAL BLOOD FLOW
- Dehydration
- Hemorrhage
- HF
- Decreased CO

• These decrease GFR and may cause oliguria (<400 mL/day)
• Prerenal Oliguria THERE IS NO DAMAGE TO KIDNEY TISSUE (PARENCHYMA). Caused by decreased blood volume
• Decreased blood volume activates angiotensin 2, aldosterone, norepinephrine, and ADH to conserve blood flow to essential organs.
• PRERENAL AZOTEMIA RESULTS IN REDUCTION OF EXCRETION OF SODIUM (<20 mEq/L), increased salt and water retention, and decreased UO.
• Prerenal conditions may cause ischemia to the kidneys and causing intrarenal damage

Question 23

Acute Tubular Necrosis

Answer 23

• Death of tubular epithelial cells
• Presents as AKI
• Caused by low blood pressure (ischemia) or nephrotoxic drugs

Question 24

AKI

Answer 24

Kidneys
- Remove waste, regulate electrolyte balance, regulate water levels, produce hormones.

• AKI causes buildup of potassium, azotemia (nitrogen containing molecules), acids in the blood due to lack of filtration ability.
• BUN to Creatinine Ratio 10-20 : 1

Question 25

Management of Renal Failure

Answer 25

• Critically ill patients have higher metabolic rates than normal to attempt to recover from the disease (many septic or hypotensive)
• Vasoactive drugs and continued waste clearance while also receiving large volumes of fluid with other medications such as nutritional/inotropic agents to treat hypotension.
• INTERMITTEN HEMODYALSIS (removing large amounts of plasma) is not indicated due to risk of worsening hypotension.

RENAL REPLACEMENT THERAPY
- Removes water/waste gently to cause little/no hypotension (Continuous renal replacement therapy - CRRT)

Question 26

Types of Renal Replacement Therapy

Answer 26

• Venovenous Hemodialysis
• Continuous venovenous hemofiltration
• Continuous venovenous hemodiafiltration
• Slow continuous ultrafiltration

Question 27

Nursing Care for CRRT

Answer 27

Monitor Vascular Access
- Due to being slow it is likely to clot

Weigh patient daily to assess fluid removal

Anticoagulation during CRRT can lead to bleeding (monitor bleeding and coagulation studies regularly)

Prevent hypothermia (blood may become cool when outside of the body). Blood warmers can be used or warming blanket.

BUN/Creatinine Levels Daily

Monitor CBC for blood loss

Check electrolyte levels because they are filtered out by CRRT (especially hypophosphatemia, which can be treated with supplements)

Question 28

GI Failure

Answer 28

• Abdominal distention and ascites
• Paralytic ileus
• GI Bleed and stress ulcers

INTERVENTION
- NG tube for decompression
- Stress ulcer prophylaxis with PPI or H2 Blockers (pantoprazole/omeprazole or famotidine)
- Monitor bowel sounds, stools
- Monitor abdominal girth, and blood in stool or NG drainage.

Question 29

Hepatic Failure

Answer 29

• “Shocked Liver”
• Manifested by elevated liver enzymes, bilirubin, coagulation defects, failure to excrete toxins such as ammonia (leads to encephalopathy)

Causes Impaired
- Albumin synthesis
- Clotting factor synthesis
- Drug metabolism

• Liver failure can lead to impaired mitochondrial function and ability for cells to use oxygen.

Question 30

Clinical Manifestations of Hepatic Failure

Answer 30

• Jaundice
• Portal Hypertension
• Hepatomegaly
• Splenomegaly
• Ascites/Varices
• GI Hemorrhage
• Encephalopathy

Question 31

Hepatic Encephalopathy

Answer 31

• Blood shunted around liver to systemic circulation allowing toxins absorbed by GI tract to circulate freely to the brain

MANIFESTATIONS
- Impaired cerebral function
- Flapping Tremors (Asterixis)
- ECG Changes

• Ammonia is the end product of intestinal protein digestion and it alters cerebral energy when it reaches the brain (metabolism and neurotransmitters)

MANIFESTATIONS
- Personality change, memory loss, irritability, lethargy (initial)
- Confusion, flapping tremor of hands, stupor, convulsions, coma (later)
- Death

Question 32

Hematologic Failure

Answer 32

Consists of
- DIC (Disseminated intravascular coagulation)
- Thrombocytopenia

Question 33

DIC

Answer 33

• Abnormally initiated accelerated clotting
• Clots and platelets go to site of action, it becomes uncontrollable where clots form in the blood vessels, clot factor proteins are completely used up, then bleeding becomes problematic.

PEOPLE AT RISK
- Infection
- Massive tissue injury
- Obstetric injury
- Vascular/Circulatory collapse
- Shock
- Transfusion Reaction
- Malignancy

Question 34

Manifestations of DIC

Answer 34

• Sepsis
• Trauma
• Blood transfusions
• Malignancy
• Liver Dysfunction
• Recent pregnancy with retained placenta

Question 35

Nursing Assessment for DIC

Answer 35

• Abnormal clotting
• Cool mottled extremities
• Dyspnea
• Multiple Sclerosis
• Decreased Urine Output
• Abnormal bleeding (oozing from site)
• Altered VS

Question 36

DIC Diagnostics

Answer 36

• Decreased platelets, fibrinogen
• Elevated D-Dimer
• PT and PTT prolonged

Question 37

Collaborative and Nursing Care DIC

Answer 37

• Treat underlying disorder
• Fluids, O2
• Replace blood, FFP, platelets
• Monitor for ischemia, fluid status, vascular occlusion

Question 38

Immunologic Failure

Answer 38

• Infection
• Decreased Lymphocyte count
• Important in sepsis patients because of extensive depletion of immune effector cells and potential immunosuppressive effect of apoptotic cells on immune system.
• Septic patients die because of severe loss of CD4 and CD8 lymphocytes
• Circulating lymphocyte subset count is a biomarker of clinical outcomes of a patient
• ANERGY - Absence of normal immune function to antigen/allergen