Sepsis Flashcards
ACID-BASE BALANCE
The process of regulatingthe pH, bicarbonateconcentration, and partialpressure of carbon dioxideof the body fluids
Regulated through respiratory and renal functions
GAS EXCHANGE CONCEPT
The process by which oxygen is transported to the cells and carbon dioxide is transported from the cells
PERFUSION CONCEPT-
pumps, pipes, and volume
The flow of blood through arteries and capillaries delivering nutrients and oxygen to cells and removing cellular wastes
IMMUNITY CONCEPT
A physiologic process that provides an individual with protection or defense from disease
Lab values for SIRS and Sepsis Spectrum
CBC (H&H, WBC, Platelet)
CMP
ABG
Procalcitonin
Lactate
PT
CRP AND CPK
WBC
5000-10000
Bands WBC > 10%
blood has a lot of immature WBCs circulating
- shift to the left
< 100000 platelets
thrombocytopenia
Albumin
3.4-5.4 pulls fluid into intravascular supporting
Total Protein normal
6-8.3 g
BUN normal
6-20
CR normal
0.6-1.3
BUN and CR measure
kidney function
Total Bilirubin normal
0.1-1.2
Procalcitonin normal
<0.1
Procalcitonin increases
when there is an infection present
Procalcitonin rises within _____________ of inflammation
2-4 hours
If procalcitonin is present, then it can help
identify tx methods
Lactic acid normal
<1
Lactic acid excess is made when
Excess production from tissue hypoperfusion (anaerobic metabolism)
Lactic acid elevated levels have a strong association with
high mortality rates
Lactate serves as
metabolic fuel for the heart and brain when the body is stressed which correlates with illness severity
PT reflects
time to clot
aPTT is more sensitive to monitor
heparin therapy
CRP (C reactive protein)
measures inflammtion
Creatine Phosphokinase
(CPK or CK) ELEVATIONS
related to injury (inflammation) or stress on muscle tissue, the heart, or the brain
CPK is released into the bloodstream when
muscles are damaged
- MI
Inflammation activates
macrophages, neutrophils, platelets to the area which causes the endothelium (lining of the vessels) to release cytokines which activate the inflammatory pathways
Neutrophils
50-70%
- first responders
- fight injury/infection
Bands
< 10%
- Babies
- immature neutrophils
- if increase, then very sick and has been sick for a while
Eosinophils
1-5%
- parasite fighters
Basophils
1%
- non-specific immune response (asthma)
- release histamines
Lymphocytes
20-40%
- B and T cells
- humoral immunity (antibodies against specific antigens)
Monocytes
2-8%
- migrate to tissues and clean up dead cells
Mast Cells
- immune cells
- connective tissue cells that contain histamine
If bands are elevated in a serum blood draw, we call this
a shift to the left
- infection
- inflammation
- release WBCs before they are fully mature
Inflammation Patho
1) Tissue injury
2)
- Capillary widening = increased blood flow
- Increased permeability = fluid release into tissues
- attraction of leukocytes = extravasation of leukocytes to site of injury
- systemic reaction = fever and proliferation of leukocytes
3) Heat, redness, swelling, tenderness, and pain
SIRS patho
1) Chemical messengers release widespread histamine
2) Widespread separation of endothelial cells = vasodilation
3) Increased blood flow = need for greater CO = TACHYCARDIA
4) increased need for O2 = TACHYPNEA = HYPOCAPNIA
5) LEUKOCYTOSIS initially and then as the WBCs are decreased = LEUKOPENIA = increased production = increased immature WBCs in blood (bands) = shift to the left
6) immune response stimulated = “thermostat” of hypothalamus altered = HYPERTHERMIA(Proper response) or HYPOTHERMIA (Improper response)
What type of concepts happen in SIRS?
Oxygenation - disrupted gas exchange
Perfusion - vasoconstriction/dilation = Tachycardia/Tachypnea/Hypocapnia
Immunity - leukocytosis/leukopenia
Thermoregulation = high or low
SIRS
Systemic inflammatory response syndrome
SIRS caused by
stressors that are either infectious or noninfectious that cause acute inflammation
SIRS defined by the presence of 2 or more of the following:
- T > 100.5 º F (38º C) or < 96.8º F (36º C)
- HR > 90
- RR > 20 or PaCO2 < 32
- WBC >12000 or <4000 or > 10% immature bands
Causes of SIRS
infection/sepsis, trauma, pancreatitis, burns, embolism, burns, shock states, distal perfusion deficits
The cytokine release (endotoxins) leads to
destruction rather than protection.
SIRS Nursing Mgmt
- maintain tissue oxygenation
Monitor labs
Hemoglobin >7
Sleep
Maintain room to encourage sleep
Administer sedation as ordered
cluster care and facilitate rest environment
SIRS Nursing Mgmt
prevent and tx infection
Advocate for removal of lines ASAP
Urinary catheters
CVL
SIRS Nursing Mgmt
- mobility
Encourage mobility
Active ROM (Walking)
Passive ROM
if tolerated
SIRS Nursing Mgmt
- nutrition and metabolic support
Start within 24 hours of admission
Enteral feeding best
Tube feedings (NGT, OGT)
Parenteral (IV) may be needed if enteral contraindicated – PEG, TPN
SIRS Tx
id and tx the primary cause
infection control (antibiotics, antivirals, antifungals)
inflammatory control
glucose control
If the cause is infectious, treat with
Bacterial, viral, fungal
If the cause is non-infectious, treat with
control s/s
Dehydration tx
crystalloids IV fluids
DM tx
control BS
RA tx
methotrexate to lower immunity
Lupus tx
control inflammation
Narrow-spectrum antibiotics
vancomycin
Broad-spectrum antibiotics
- levofloxacin, piperacillin/tazobactam (zocen), ceftriaxone, meropenem, cefepime
Inflammatory control
Glucocorticoids: hydrocortisone, dexamethasone, methylprednisolone, prednisone
Tylenol
Glucose control
maintain <180 mg/dL – insulin scheduled or drip
Antivirals
oseltamivir (Tamiflu), interferon, acyclovir
Antifungals
amphotericin, nystatin
Is sepsis contagious?
no
- blood infection
Risk Factors to sepsis
Invasive devices/lines
Extremes of age (elderly/very young)
Malignancies
Burns
AIDS
Diabetes
Substance abuse
Wounds
Immunosuppressive therapy
Inflammation and coagulation linked in Sepsis patho
Inflammation > Coagulation pathways forms thrombin (clots) > tiny clots (microthrombi) > blocks blood flow to organs > hypoxia or hypoperfusion to organs>eventually fibrinolysis occurs (breakdown of clots) but can use up all fibrin available, so they have clots all over.
Infection + change in
Sepsis-related
Organ
Failure
Assessment
> 2 systems (cardiac, respiratory, neuro, kidney, liver, hematologic)
Sepsis Assessment of Organ System
low PaO2/FiO2
low BP or vasopressors
low platelets
low GCS
high bilirubin
high creatinine and oliguria
PaO2/FiO2 Ratio**
300-500
= normal
PaO2/FiO2 Ratio**
200-300
= acute lung injury
PaO2/FiO2 Ratio**
<200
= significant lung injury
PaO2/FiO2 Ratio**
<100
= High mortality
Hypotension
< 90/60
MAP
< 70
Thrombocytopenia
<150,000
GCS change in sepsis
<14
<8 intubate
GCS measures
eye
motor
verbal
(table has a GCS of 3)
Bilirubin sepsis
> 1.2
Creatinine and urine output in sepsis
> 1.2 BUN
< 500mL/day - oliguria
Sepsis Nursing Mgmt
Assess perfusion & oxygenation – cap refill <3
Early identification of SIRS - trends
Assess need for fluid resuscitation
- passive leg raises (HOB flat and legs in the air
- internal bolus 450
Monitor effectiveness, I&Os, daily wt, labs (Procalcitonin and lactate)
Maintain bedrest
After assessing for a fluid resusciatation, the BP raises
responsive and needs fluid
If septic, then the fluid should be
30mL/kg/hr
Effectiveness of fluid resuscitation if
Vital signs – increase BP
Capillary refill 2-3 seconds
Skin temperature warm
Urine output >0.5 mL/kg/hr
Central venous pressure (CVP) 8-12 mmHg
MAP >65 mmHg
Sepsis Tx
administer crystalloid bolus
blood cultures
antibiotics quickly within 3 hours
lactate levels
Vasopressors
When do you give a crystalloid bolus
hypotension and/or lactate>2
- 30 mL/kg
Administer as quickly as the patient can tolerate
Max of 3 hours for sepsis
Max of 1 hour for septic shock
How long does it take blood cultures to grow
2-4 days
recommended time to start antibiotics for septic shock
1 hour
Continue antibiotic tx until
WBC<10000
Repeat lactate acid if >
2
Give what if fluid is not effective
vasopressors
- Norepinephrine then vasopressin (antidiuretic)
NS is
acidic
Septic shock criteria
SIRS plus a confirmed infection
MAP < 65 MMHG
Serum Lactate ≥ 2 MMOL/L
Vasopressors
Organ Dysfunction
Septic shock is the stage of
sepsis when MODS and organ failure are evident AND poor clotting with uncontrolled bleeding can occur.
- severe hypovolemic shock and hypodynamic cardiac function present
sepsis on steroids
Massive vasodilation
Increased vessel diameter & permeability
Decreased systemic vascular resistance (SVR)
Decrease in blood pressure
Initially increased Cardiac Output (CO) to compensate for decreased SVR
Continual feedback causes decreased CO
WARM skin initially but as progresses will become COOL
Damage to vessels systemically causing
coagulation factors to clot
Eventually clotting factors used up
Causing disseminated intravascular coagulopathy (DIC)
Hypoperfusion
= Organs not receiving oxygen and an anaerobic metabolism occurs
Lactic acid produced and levels begin to rise rapidly
Respiratory blood vessels damaged cause
Acute respiratory distress syndrome (ARDS)
Severe hypoxemia
Need to be mechanically ventilated
What happens to the body when septic shock occurs?
Increased WBC to area all throughout the body
Vessels increase in diameter due to the increased WBCs and other molecules called to the intravascular space
Vessels become more permeable and begin to leak fluid into the interstitial tissue space (decreased systemic vascular resistance SVR) which decreases BP
This increased fluid cause issues with oxygen transport to tissues
The endotoxins from the WBC damage the blood vessels
Coagulation cascade starts and begins to try to clot to repair the blood vessel damage
Clots can break off in the blood stream (what would happen?)
When we run out of clotting factors, the patient begins to bleed everywhere which is DIC
Cardiac output initially increases to try to compensate for the drop in blood pressure, but eventually due to lack of oxygen it will also lose the ability to compensate so CO decreases
S/S resemble the late stage of
hypovolemic shock
Septic Shock Nursing Mgmt
Cardiac – SBP <90 and/or MAP <65
Respiratory failure and need for mechanical ventilation
- Blood cultures
Lactate (Lactic Acid)
Repeat if ≥2 mmol/L
PaO2 <60
Kidneys: Creatinine >2.0 or Urine output <0.5 mL/kg/hr
Liver: Bilirubin >2 mg/dL
Hematology:
Platelets <100,000
INR >1.5 or PTT > 60 seconds
Inflammatory markers: C-Reactive Protein (CRP) & Erythrocyte Sedimentation Rate (ESR)
What do you do after getting lactic acid labs?
put on ice immediately
Septic Shock Tx
Fluid Resuscitation
30 mL/kg
Add vasopressors if fluid resuscitation is not effective
norepinephrine, vasopressin, phenylephrine, dopamine
vasoconstrictors may decrease coronary artery perfusion so monitor for chest pain or pressure
Used to increase blood pressure due to decreased systemic vascular resistance (SVR)
Maintain PaO2 >75 prefer 80
Monitor lactate levels to determine hypoperfusion
Broad spectrum antibiotics
Can narrow down once cultures come back
Disseminated Intravascular Coagulation (DIC) patho
Tissue damage/endothelial injury
Clotting stimulated - Microvascular thrombi
(everywhere in the body)
Body tries to break down clots - Fibrinolytic mediators are released
Chaos occurs
Clots are forming - body trying to break down clots – results in consumption of clotting factors
Ability to clot is lost
Bleeding occurs
Initial DIC S/S
Excessive Clotting
(Lasts hours to weeks)
Ischemic toes, fingers &/or tip of nose
DIC S/S may progress to
Thrombosis
Gangrene
Altered LOC, CVA
SOB, PE
Bowel ischemia/ infarction
Acute renal failure
DIC S/S leads to excessive bleeding by
Bleeding from various sites
Petechiae
Hematuria
Oozing from IV sites
GI bleeding
Oozing gums
Initially DIC is what type of shock
obstructive
Late DIC is what type of shock
hypovolemia
Petechiae
bruising spots under the skin
DIC Lab Values
low fibrinogen and platelet count
high PTT and PT
high D-Dimer
Fibrinogen
converted to thrombin to form a clot; as body converts, fibrinogen levels will decrease
Platelets
body trying to form lots of clots, so circulating platelet levels decrease to less than 100,000 µL usually closer to 50,000
PT normal
10-13 seconds
PTT normal
25-35 seconds.
PT and aPTT will be prolonged.
D-Dimer
fibrin degradation product – small protein present after a blood clot is degraded by fibrinolysis.
D-dimer will be elevated.
DIC Mgmt
Prevent or control hemorrhaging
Identify the cause
Assess patient for bleeding
thrombocytopenia
petechiae
bruising
black or tarry stools
Teach patient about precautions with DIC
Thrombocytopenia: Goal
prevent or control hemorrhaging
Assessment for bleeding or clotting includes
Black or tarry stools
Black or coffee ground emesis
Black or bloody sputum or urine
Bleeding from anywhere on the body that will not stop
Headache or changes in vision
Petechiae
Cap refill prolonged
Teachings for DIC
Avoid medications that can prolong bleeding such as aspirin or ibuprofen**
Avoid garlic as this herb increases bleeding**
Do not blow nose forcefully – tendency for nosebleed that will not stop.
Do not bend down with head lower than waist – increases ICP and could cause hemorrhagic bleed in brain.
Do not use a suppository, enema, or tampons**
Pain in legs or extremities, mixed temperatures let me know = DVT
Prior to transfusion what should the nurse do
Verify the order.
Obtain or review patient signed consent form (Plasma, platelets, cryo, RBC)
Physician tells them about it
Witness signature
Set-up for Blood Transfusion
Use blood filter tubing and prime above the filter with 0.9% NS through all tubing.
Only use NS to prime and clean line with all blood products.
Fluids containing glucose are not compatible with red blood cells and cause the RBCs to clump.
Crystalloid or colloid solutions that contain calcium should never be administered concurrently with any blood product as calcium revers the anticoagulant citrate causing RBCs to clot.
What should the nurse monitor during the transfusion?
Monitor patients closely when you start blood products.
Vital signs should be done prior to transfusion, 15 mins after start, and at the completion
Average duration of infusion of blood products:
RBC 1.5-3 hours
Platelets 30-60 mins as tolerated
FFP 30-90 mins
Cryoprecipitate 30 mins or less
Maximum infusion time is 4 hours
Change tubing every 4 hours
DOCUMENT
Vital signs (pre, 15 mins, and completion)
Start and stop time of infusion
Volume infused
Evidence of transfusion reaction or suspected reaction or no evidence of reaction
NEVER EVER SHOULD THESE BE DONE WITH BLOOD OR BLOOD PRODUCTS:
Attempt to manipulate the temperature of the unit by running under warm water or putting it in the microwave.
Contact the blood bank if it needs to warmed
Store blood components in an unmonitored refrigerator (ex: staff or patient refrigerators)
Add medications to the blood bag or line or piggy back any medications or other products
This could hemolyze or clot the blood
If they have reactions, then
stop and disconnect tubing and notify someone
Plasma
Filtered portion that provides volume, coagulation factors and other proteins
Platelets
Small fragments (thrombocytes) that control bleeding
Cryoprecipitate
Concentrated levels of fibrinogen and clotting factors from multiple donors
Red blood cells
Contain hemoglobin but NO clotting factors
Replaces volume and oxygen carrying components
MUST use blood tubing with filter and prime with 0.9% sodium chloride
MUST BE CROSSMATCHED
Albumin –
Does not require patient consent
Large protein to pull fluid back into the vessels
Increases intravascular volume
Multiple Organ Dysfunction Syndrome (MODS)
Progressive compensation leads to severe organ dysfunction and eventually failure and death
- no homeostasis w/o intervention
Most common trigger for MODS
septic event
MODS is what type of problem
Perfusion – organs not being perfused – hypoperfusion occurs, anaerobic metabolism due to low or no oxygen, organs start to shut down.
MODS: Pulmonary Dysfunction S/S
Tachypnea
1st organ initiating MODS cascade
Dyspnea
Shallow breathing
Hypoxemia
Crackles
ABG <70 PaO2 or > 50 PaCO2
PaO2/FiO2 <200
Respiratory failure with high FiO2
Mechanical Ventilation
1st organ initiating MODS cascade
Respiratory - Tachypnea
MODS: Pulmonary Dysfunction PATHO
Hypoxemia develops causing an increased drive for ventilation.
The lungs are stiff due to the inflammation in the alveoli.
Inflammation in the alveoli starts when there is reduced blood flow to the lungs, histamine is released which increases the permeability of the alveoli, and fluid shifts into the interstitial space.
This permeability allows proteins and fluids to leak out which increases the osmotic pressure and causes pulmonary edema.
As the fluid builds up, there is decreased space for O2 to exchange because of the damaged alveolocapillary membrane, but CO2 can cross the membrane.
Not having enough oxygen in the alveoli, leads to hypoperfusion of other organs, increasing the lactate level which is a byproduct of anaerobic metabolism due to low levels of oxygen in the tissues.
MODS: Pulmonary Dysfunction Dx
Bilateral infiltrates on chest Xray
ABG: Respiratory alkalosis
Hypocapnia
Hypoxemia
MODS: Pulmonary Dysfunction mgmt
Frequent respiratory assessment – rate, depth, position
Maintain lowest FiO2 to maintain PaO2 >75 mmHg prefer 80 mmHg
Adjust environment to decrease oxygen intense activities
MODS: Pulmonary Dysfunction tx
Treat hypotension with fluid and/or vasopressors
Mechanical ventilation may be needed
MODS: CV Dysfunction S/S
Tachycardia
Hypotension
Capillary refill > 4
Skin mottling
Cool skin
Weak pulse
MAP < 65 mm HG
Low SVR
Dysrhythmias
Electrolytes: Hyperkalemia > Peaked T waves
BP < 90/60
SBP <90 mm Hg
Decrease more than 40 points from baseline
MODS: CV Dysfunction PATHO
Inflammation causes vasodilation.
Vasodilation causes hypotension:
Mean Arterial Pressure (MAP) <75 mm Hg
Low Systemic vascular resistance (SVR)
Tachycardia causing increased cardiac output and stroke volume
Myocardial depression happens when systolic and diastolic dysfunction occurs affecting both sides of the heart.
Right side gas exchange issues.
Left side perfusion issues all related to the vasodilation due to inflammation.
MODS: CV Dysfunction MGMT
Cardiac assessment – tachypnea, edema, signs of hypoperfusion (cap refill, mottling)
Monitor ECG for dysrhythmias
MODS: CV Dysfunction TX
Maintain MAP > 75 mmHg
Fluid resuscitation
Vasopressors (norepinephrine, dopamine, epinephrine, phenylephrine)
Treat electrolyte disturbances
MODS: NEURO Dysfunction S/S
Confusion/delirium
Headache
Agitation
Lethargy
Seizures
No cough/gag reflex
Slow or no pupil response
Pupils mid-position and dilated (4-9 mm)
GCS <8 (Coma)
MODS: NEURO Dysfunction PATHO
Both inflammatory and non-inflammatory processes cause significant alterations in the brain.
There is impaired cerebral perfusion from prolonged inflammation, severe hypoxemia, and persistent hyperglycemia.
It is the pro inflammatory mediators that relay the message to begin the inflammatory process which disrupts the microcirculatory system and compromises cerebral perfusion.
If left untreated, may result in encephalopathy or acute cerebrovascular lesions.
MODS: NEURO Dysfunction MGMT
Control the factors that affect the brain:
Thermoregulation
Glucose control
Hemodynamic regulation (blood pressure and oxygenation)
Adjusting the environment – low noise and lights to decrease stimulation
MODS: NEURO Dysfunction TX
benzos or opioids causing CNS sedation
diuretics causing dehydration
steroids altering the serotonin activity
MODS: RENAL Dysfunction S/S
Oliguria leading to possible anuria
Fluid retention
Urine output < 0.5 mL/kg/hr
Hyperkalemia >5.5
Hematuria
Proteinuria
Creatinine >1.2
MODS: RENAL Dysfunction PATHO
Decreased perfusion to the kidneys due to gas exchange and perfusion issues activates the renin-angiotensin system.
Renin forms angiotensin I which is then converted to the vasopressor angiotensin II.
AGII raises low blood pressure by increasing peripheral vasoconstriction and stimulating aldosterone secretion.
Aldosterone promotes the reabsorption of water and sodium to correct the fluid deficit and inadequate blood flow causing renal ischemia.
The body is trying to protect itself from something that it has caused as a result of the original infarct or injury.
MODS: RENAL Dysfunction MGMT
Monitor urine output - >0.5 mL/kg/hr.
Monitor labs – creatinine elevations
Assess for hematuria, proteinuria, edema, crackles lungs, dehydration, hypokalemia/hyperkalemia
MODS: RENAL Dysfunction TX
Treatment:
Restore perfusion via fluid resuscitation and/or vasopressors
MODS: LIVER Dysfunction S/S
Jaundice
Confusion
Edema
Fatigue
Nausea
Upper abdominal pain
Coagulation disorders
Hyperbilirubinemia > 2 mg/dL
Hyperammonemia
>82 mcg/dL Females
>94 mcg/dL Males
Hypoalbuminemia <2 g/dL
Elevated AST and ALT
Hepatic encephalopathy
MODS: LIVER Dysfunction PATHO
Due to widespread organ hypoperfusion, the liver is unable to transport bile acids and bilirubin to the hepatic canaliculi, which causes cholestasis.
Lactate is not able to be cleared through the liver.
Protein synthesis is also reduced (specially albumin) which causes hypoalbuminemia which the body loses the oncotic pull into the vascular system and widespread edema can occur.
The liver cannot produce glucose which can cause hypoglycemia.
MODS: LIVER Dysfunction TX
Lactulose for hyperammonemia
Blood transfusions:
Albumin
Packed RBCs
Clotting factors
UV therapy
MODS: GI Dysfunction S/S
Abdominal pain
Distention
Hypoactive bowel sounds
No bowel sounds
Tarry stool
Bright red stool
Peristalsis leading to ileus
Permeability of GI tract
Bacterial translocation
MODS: GI Dysfunction PATHO
In the early stages of SIRS and MODS, blood is shunted away from the GI mucosa, making it highly vulnerable to ischemic injury.
Mucosal ischemia leads to a breakdown of this normally protective mucosal barrier.
Hypoperfusion decreases peristalsis and eventually causes paralytic ileus.
This increases the risk for ulceration, GI bleeding, and bacterial movement from the GI tract into circulation.
The gut has bacteria that is supposed to help us like low levels of Clostridium difficile and E. Coli.
If they move outside of the intestines, it has severe consequences throughout the body.
MODS: GI Dysfunction MGMT
Monitor for abdominal distention, peristalsis, or ileus.
Enteral feedings – start within 24 hours
NGT, OGT or Jejunostomy tube
Stop if ileus
MODS: ENDOCRINE Dysfunction TX
Proton pump inhibitors (pantoprazole)
Monitor for effectiveness or adverse effects.
Mobility – either active/passive ROM, walking
MODS: ENDOCRINE Dysfunction S/S
Hyperglycemia
Hot & Dry “sugar high”
Thirsty with polyuria, irritable, stomach pain, dry mouth
Hypoglycemia
Cold and clammy “need some candy”
Lethargic, pallor, hungry
Decreased wound healing
- CLEAR URINE
180 BLOOD SUGAR IS OKAY IN SEPSIS DUE TO STRESS
MODS: ENDOCRINE Dysfunction PATHO
The adrenal glands and the pancreas are two that play a role in endocrine regulation.
When there is inflammation or stress on the body, the hypothalamus signals the production of hormones such as glucocorticoids (anti-inflammatory and controls metabolism) and catecholamines (ex: dopamine and epinephrine; stimulates the heart, raises blood pressure) and both are regulated from adrenal glands.
The pancreas secretes insulin, amylase, and lipase. These are responsible for controlling glucose needs in the body.
MODS: ENDOCRINE Dysfunction MGMT
Maintain glucose control
MODS: ENDOCRINE Dysfunction TX
Treatment:
Insulin protocol
Insulin drip to maintain glucose <180 mg/dL
MODS: BLOOD AND METABOLIC Dysfunction
Thrombocytopenia
Platelet count < 100,000 microliters
Coagulopathy
Decreased Fibrinogen
INR > 1.5 or PTT > 60 seconds
Increased D-dimer
Lactate > 2 mmol/L
Metabolic acidosis
- LOW pH and HCO3
MODS Mgmt
Provide hemodynamic monitoring
- MAP 70-105
Maintain strict I & O/Daily weight
Monitor labs closely
Assess central lines daily and change dressing prn
Assist with aggressive pulmonary management
Ambulation or passive ROM
TCDB
Oral care
MODS has no chance of returning to normal
false
Which patient manifestations confirm the development of MODS?
A
Upper GI bleed, Glasgow Coma Scale score of 13, and Hct of 35%
B
Elevated serum bilirubin, serum creatinine of 3.8 mg/dL, and platelet count of 15,000
C
Urine output of 30 mL/hr, BUN 25 mg/dL, and WBC of 6120
D
Respiratory rate of 25 bpm, PaCO2 of 45 mmHg and CXR with bilateral diffuse patchy infiltrates
B
Elevated serum bilirubin, serum creatinine of 3.8 mg/dL, and platelet count of 15,000
2 or more organs are failing. Bilirubin indicates liver dysfunction, serum creatinine of 3.8 indicates kidney injury and platelets of 15,000 indicates hematologic failure.
MODS Tx
prevention and treatment of infection
- Remove sources of infection: foley, central lines - Cultures - Antibiotics
Increase supply: FiO2, Hgb
Decrease demand: sedation, rest, cluster care, maintain normal temp
Enteral nutrition within 24 hours
Glycemic control 140-180 mg/dL
Perfusion - vasopressors, fluid
CNS – benzos, opioids, diuretics, steroids
blood transfusions (albumin, PRBC)
proton pump inhibitors (Pantoprazole)
insulin therapy
