5.2 Complications of Shock Flashcards
1
Q
MODS (Multiple Organ Dysfunction Syndrome)
A
- 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.
2
Q
MODS
A
- 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
3
Q
Deitch Theory Gut Hypothesis
A
- 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
4
Q
MODS Criteria
A
- Presence of 2+ organ dysfunction in acutely ill patients requiring intervention
- Can be primary or secondary
- High mortality rate
5
Q
MODS Treatment
A
- Control initiating event
- Promoting adequate organ perfusion
- Provide adequate nutrition
- Promote communication
6
Q
Progression of MODS
A
- Inflammatory response leads to hypermetabolism and misdistribution of blood flow which causes perfusion issues and organ damage/cell death.
7
Q
Primary (Early) MODS
A
- Local and generalized hypoperfusion triggers inflammatory and stress responses
8
Q
Secondary (Late) MODS
A
- Excessive inflammatory response manifested in organs distant from original injury
- Activates inflammatory response, coagulation, and fibrinolysis
9
Q
Manifestations of MODS
A
- Respiratory failure within first 72 hours
- Liver failure 5-7 days after injury
- GI Bleed 10-15 days
- Renal failure 11-17 days
10
Q
Pulmonary Manifestations
A
- Dyspnea
- Refractory Hypoxemia
- Respiratory Acidosis
- Abnormal O2 Indices
- Patchy Infiltrates
- Pulmonary Hypertension
11
Q
GI Manifestations
A
- Mucosal Ulcerations
- Abdominal distension and ascites
- Bacterial overgrowth in stool
- GI BLEEDING
- Paralytic Ileus
- Intolerance of Enteral Feedings
12
Q
Liver
A
- Increased bilirubin, liver enzymes, serum ammonia
- Jaundice
- Hepatomegaly
13
Q
Cardiovascular (Hyperdynamic)
A
- Increased o2 consumption, cardiac output, cardiac index, heart rate
- Decreased pulmonary capillary wedge pressure (PCWP), SVR, right atrial pressure
14
Q
Cardiovascular (Hypodynamic)
A
- Increased SVR, right atrial pressure, left ventricular stroke work index
Decreased oxygen delivery/consumption, cardiac output, cardiac index
15
Q
Metabolic/Nutritional
A
- Muscle wasting, Weight loss, Decreased lean body mass
- Increased serum lactate
- Decreased serum albumin
- Hyperglycemia/Hypertriglyceridemia
- Negative nitrogen balance
16
Q
Renal
A
- Increased serum creatinine and BUN
- Oliguria/Anuria
- Possible polyuria
- Acute tubular necrosis
17
Q
CNS
A
- Lethargy/LOC
- Fever
- Hepatic Encephalopathy
18
Q
Coagulation/Hematologic
A
- Thrombocytopenia
- Disseminated Intravascular Coagulation (DIC)
19
Q
Immune
A
- Infection
- Decreased lymphocyte count
- Anergy (absence of normal immune response to specific antigens/allergens)
20
Q
ARDS (Acute Respiratory Distress Syndrome)
A
- RESPIRATORY SYSTEM IS THE FIRST TO FAIL
21
Q
Causes of Renal Failure
A
- 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)
22
Q
Prerenal Causes
A
- 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
23
Q
Acute Tubular Necrosis
A
- Death of tubular epithelial cells
- Presents as AKI
- Caused by low blood pressure (ischemia) or nephrotoxic drugs
24
Q
AKI
A
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
25
Management of Renal Failure
- 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)
26
Types of Renal Replacement Therapy
- Venovenous Hemodialysis
- Continuous venovenous hemofiltration
- Continuous venovenous hemodiafiltration
- Slow continuous ultrafiltration
27
Nursing Care for CRRT
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)
28
GI Failure
- 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.
29
Hepatic Failure
- "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.
30
Clinical Manifestations of Hepatic Failure
- Jaundice
- Portal Hypertension
- Hepatomegaly
- Splenomegaly
- Ascites/Varices
- GI Hemorrhage
- Encephalopathy
31
Hepatic Encephalopathy
- 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
32
Hematologic Failure
Consists of
- DIC (Disseminated intravascular coagulation)
- Thrombocytopenia
33
DIC
- 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
34
Manifestations of DIC
- Sepsis
- Trauma
- Blood transfusions
- Malignancy
- Liver Dysfunction
- Recent pregnancy with retained placenta
35
Nursing Assessment for DIC
- Abnormal clotting
- Cool mottled extremities
- Dyspnea
- Multiple Sclerosis
- Decreased Urine Output
- Abnormal bleeding (oozing from site)
- Altered VS
36
DIC Diagnostics
- Decreased platelets, fibrinogen
- Elevated D-Dimer
- PT and PTT prolonged
37
Collaborative and Nursing Care DIC
- Treat underlying disorder
- Fluids, O2
- Replace blood, FFP, platelets
- Monitor for ischemia, fluid status, vascular occlusion
38
Immunologic Failure
- 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
