Week 15: Impaired Immunity

Question 1

Systemic inflammatory response syndrome (SIRS), triggers, criteria needed, what does it advance to?

Answer 1

*Generalized inflammation in organs remote from initial insult

*Consider fairly reversible. Problem is that it advances to MONS

Criteria (2 or more needed):

• Fever greater than 38.0 or less than 36
• hr greater than 90
• RR greater than 20
• WBC above 12,000, less than 4,000
• Bands greater than 10%

Triggers

• Mechanical tissue trauma: burns, crush injuries, surgical procedures
• Abscess formation: intra-abdominal, extremities
• Ischemic or necrotic tissue: pancreatitis, vascular disease, MI
• Microbial invasion: Bacteria, viruses, fungi
• Endotoxin release: Gram-negative bacteria
• Global perfusion deficits: Post–cardiac resuscitation, shock states
• Regional perfusion deficits: Distal perfusion deficits

Question 2

Multiple organ dysfunction syndrome (MODS)

Answer 2

• failure of two or more organ systems
• Homeostasis cannot be maintained without intervention-Results from SIRS
• SIRS and MODS represent ends of a continuum
• Transition from SIRS to MODS DOES NOT occur in a clear-cut manner

Question 3

Consequences of inflammatory response

Answer 3

• Low BF
• Release of mediators
• Direct damage to endothelium
• Hypermetabolism
• Vasodilation leading to dec SVR
• Inc in vascular permeability
• Activation of coagulation cascade
• Inflammation can travel to other organs and cause the same response in other organs

Question 4

SIRS and MODS patho and stages

Answer 4

• Organ and metabolic dysfunction
• Hypotension
• Decreased perfusion
• Formation of microemboli
• Redistribution or shunting of blood

Stage 1:

local cytokine relase

Stage 2:

release of cytokines into systemic system

stage 3:

Humoral cascade (clotting cascade being released systemically in multiple organs)

Question 5

SIRS/MODS in respiratory system

Answer 5

• Alveolar edema
• Decrease in surfactant
• Increase in shunt
• V/Q mismatch
• End result: ARDS
• 70% will go into MODS, so the VAP protocols are essential

Question 6

Cardiovascular system SIRS/MODS patho

Answer 6

• Myocardial depression and massive vasodilation
• decreased CO, decreased preload, increased afterload leading to ischemia to the heart
• Depressed cardiac muscle function

Question 7

Renal system SIRS/MODS patho

Answer 7

Acute renal failure

• Hypoperfusion leading to ischemia
• Release of mediators
• Activation of renin–angiotensin– aldosterone system to compensate (which causes vasoconstriction, furthering ischemia)
• Nephrotoxic drugs, especially antibiotics further the insult. Quinolines, Sulfas, Vancomycins

Question 8

GI system SIRS/MODS patho

Answer 8

• Motility decreased: Abdominal distention and paralytic ileus
• Decreased perfusion: Risk for ulceration and GI bleeding
• Potential for bacterial translocation

Hypermetabolic state

• Hyperglycemia–hypoglycemia
• Insulin resistance
• Catabolic state
• Liver dysfunction
• Lactic acidosis

Question 9

Hematologic system SIRS/MODS patho

Answer 9

• DIC
• Electrolyte imbalances
• Metabolic acidosis

Question 10

SIRS/MODS collaborative care prevention

Answer 10

• Prognosis for MODS poor
• Goal: Prevent progression of SIRS to MODS
• Vigilant assessment-ongoing monitoring to detect early signs of deterioration or organ dysfunction-critical
• Prevention and treatment of infection
  
  • Aggressive infection control strategies to dec risk for nosocomial infections
  • Once an infection suspected, institute interventions to control source !~

Question 11

SIRS/MODS collaborative care oxygenation

Answer 11

Maintain tissue oxygenation

• Dec O2 demand
  
  • Sedation
  • Mechanical ventilation (on volume control)
  • Paralysis
  • Analgesia
• Optimize O2 delivery
  
  • Maintain normal hemoglobin level
  • Maintain normal PaO2
    
    • Individualize tidal volumes with PEEP ( don’t want too much volume, can cause barotrauma)

Question 12

Maintenance of tissue oxygenation with SIRS/MODS

Answer 12

Maintenance of tissue oxygenation
Enhance CO

• Increase preload or myocardial contractility: dopamine and dobutamine
• Reduce afterload: Nipride or nitro drip,
• Give levofed to cause vasoconstriction: cuts circulation into the periphery increasing SVR and preload

Question 13

SIRS/MODS collaborative care with nutrition

Answer 13

• Nutritional and metabolic needs
• Goal of nutritional support: Preserve organ function-total energy expenditure-often inc 1.5 to 2.0 times: need HIGH PROTEIN feed.
• Nutritional and metabolic needs
• Use of enteral route preferred to parenteral nutrition
• Monitor plasma transferrin & prealbumin levels to assess hepatic protein synthesis

Question 14

SIRS/MODS failiing organs

Answer 14

Support of failing organs

• ARDS: Aggressive O2 therapy and mechanical ventilation
• DIC: Appropriate blood products
• Renal failure: Continuous renal replacement therapy or dialysis

Question 15

Shock, classifications

Answer 15

• Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism
  
  • Imbalance in supply/demand for O2 and nutrients
• Classification of shock
  Cardiogenic:
  Hypovolemic:
  Distributive:
  Obstructive:

Question 16

cardiogenic shock

Answer 16

Definition

• Systolic or diastolic dysfunction
• Compromised cardiac output (CO)

Precipitating causes

• Myocardial infarction
• Cardiomyopathy
• Blunt cardiac injury
• Severe systemic or pulmonary hypertension
• Cardiac tamponade
• Myocardial depression from metabolic problems

Question 17

patho of cardiiogenic shock

Answer 17

decrease in filling that leads to a decrease in stroke volume. Up to 85% die

CO lesss than 4 or cardiac input of less than 2.5

Question 18

Manifestations of Cardiogenic shock

Answer 18

Early manifestations

• Tachycardia; Hypotension
• Narrowed pulse pressure
• ↑ myocardial O2 consumption

Physical examination

• Tachypnea, pulmonary congestion
• Pallor; cool, clammy skin
• Dec capillary refill time
• Anxiety, confusion, agitation
• ↑ in pulmonary artery wedge pressure
• Dec renal perfusion and UO

Question 19

Absolute hypovolemia

Answer 19

loss of intravascular fluid volume

• Hemorrhage; GI loss (e.g., vomiting, diarrhea)
• Fistula drainage; Diabetes insipidus
• Hyperglycemia; Diuresis

Question 20

relative hypovolemia

Answer 20

• Results when fluid volume moves out of vascular space into extravascular space (e.g., interstitial or intracavitary space)
• Termed third spacing

Question 21

patho of hypocolemic shcok

Answer 21

• greater than 40% volume loss is irreversible and there will be permanent damage. Body tries to autoregulate, but can’t past this 40%, causing ischemia and damage to all organs
• Look at H&H, (see an increase with diabetes insipidous or third spacing, otherwise it will go down), look at electrolytes (increase in K+), ABGS, CV o2 sat, watching UO hourly (have to be cathed)

Question 22

clinical manifestations of hypovolemic shock

Answer 22

• Anxiety
• Tachypnea
• Inc in CO, heart rate
• Dec in stroke volume, PAWP, urinary output
• If loss is >30%, blood volume is replaced.

Question 23

Distributive shock/neurogenic shock and clinical manifestations

Answer 23

• Hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and last up to 6 weeks
• Can occur in response to spinal anesthesia
• Results in massive vasodilation > lead to pooling of blood in vessels

Clinical manifestations

• Hypotension
• Bradycardia
• Temperature dysregulation (resulting in heat loss) (warm skin from vasodilation, then it cools and get hypothermia)
• Dry skin
• Poikilothermia (taking on the temperature of the environment)

Question 24

distributive shock/anaphylactic shock, manifestations, treatment

Answer 24

Acute, life-threatening hypersensitivity reaction

• Massive vasodilation; Release of mediators
• ↑ capillary permeability

Clinical manifestations

• Anxiety, confusion, dizziness
• Sense of impending doom; Chest pain
• Incontinence
• Swelling of the lips and tongue, angioedema
• Wheezing, stridor; Flushing, pruritus, urticaria
• Respiratory distress and circulatory failure

Treatment

• A (establish this quick) BCDE
• If you don’t have an epi pen, have them in a position to help with vasodilation, so you want their feet elevated
• Epi (adrenaline) lasts only 20 minutes, then it needs to be repeated (give every 3-5 minutes in hospital until you get a response)
• High flow oxygen is appropriate for these patients (veni mask, face mask)
• IV fluids: Adults 500-1,000, children crisiloid 20ml/kg
• Give steroids and medications to help with allergic reactions (hydrocortisone, chloriphenamine

Question 25

Distributive/Septic shock, clinical manifestations

Answer 25

• Sepsis: systemic inflammatory response to documented or suspected infection
• Severe sepsis = Sepsis + Organ dysfunction
• Presence of sepsis with hypotension despite fluid resuscitation
• Presence of tissue perfusion abnormalities

Clinical manifestations

• ↑ coagulation and inflammation
• ↓ fibrinolysis
• Formation of microthrombi
• Obstruction of microvasculature
• Hyperdynamic state: increased CO and decreased SVR
• Tachypnea/hyperventilation
• Temperature dysregulation
• ↓ urine output
• Altered neurologic status
• GI dysfunction
• Respiratory failure common.

Question 26

obstructive shock

Answer 26

(pulmonary embolis) Develops when physical obstruction to blood flow occurs with decreased CO

• From restriction to diastolic filling of right ventricle due to compression
• Abdominal compartment syndrome

Patient experience

• Dec CO
• Increased afterload
• Variable left ventricular filling pressures

Rapid assessment and immediate treatment important

Question 27

initial stage of shock

Answer 27

• Usually not clinically apparent
• Usually considered reversible
• Metabolism changes from aerobic to anaerobic.
  
  • Lactic acid accumulates -must be removed by blood and broken down by liver.
  • Process requires unavailable O2.
• Clinically apparent –Neural, Hormonal &Biochemical compensatory mechanisms
• Attempts aimed to overcome consequences of anaerobic metabolism and maintaining homeostasis.

Question 28

compensatory (or initial?) stage of shock

Answer 28

• Baroreceptors in carotid and aortic bodies activate SNS in response to ↓ BP.
  
  • Vasoconstriction while blood to vital organs maintained-
• ↓ blood to kidneys > activates renin– angiotensin system ↑ venous return to heart, CO, BP
• Impaired GI motility- Risk for paralytic ileus
• Cool, clammy skin from blood
  
  • Except septic patient who is warm and flushed

Question 29

complensatory stage

Answer 29

• Shunting blood from lungs increases physiologic dead space.
  
  • ↓ arterial O2 levels
  • Increase in rate/depth of respirations
  • V/Q mismatch
• SNS stimulation increases myocardial O2 demands.
• If perfusion deficit corrected, patient recovers with no residual sequelae
• If deficit not corrected, patient enters progressive stage

Question 30

progressive stage of shock

Answer 30

• Begins when compensatory mechanisms fail
• Aggressive interventions to prevent multiple organ dysfunction syndrome (MODS)
• Hallmarks -↓ cellular perfusion & altered capillary permeability
  
  • Leakage of protein into interstitial space
  • ↑ systemic interstitial edema

Anasarca

• Fluid leakage affects solid organs and peripheral tissues.
• ↓ blood flow to pulmonary capillaries

Movement of fluid from pulmonary vasculature to interstitium

• Pulmonary edema
• Bronchoconstriction
• ↓ residual capacity

Fluid moves into alveoli

• Edema-Dec surfactant
• Worsening V/Q mismatch
• Tachypnea, Crackles
• Inc work of breathing

CO begins to fall

• Dec peripheral perfusion
• Hypotension
• Weak peripheral pulses
• Ischemia of distal extremities

Myocardial dysfunction results in

• Dysrhythmias
• Ischemia; Myocardial infarction
• End result: complete deterioration of cardiovascular system

Liver fails to metabolize drugs and waste.

• Jaundice; Elevated enzymes
• Loss of immune function
• Risk for DIC and significant bleeding

Mucosal barrier of GI system becomes ischemic

• Ulcers
• Bleeding
• Risk of translocation of bacteria
• Dec ability to absorb nutrients

Question 31

irreversible stage of shock

Answer 31

• Exacerbation of anaerobic metabolism
• Accumulation of lactic acid
• ↑ capillary permeability
• Profound hypotension and hypoxemia
• Tachycardia worsens.
• Failure of one organ system affects others.
• Recovery unlikely

Question 32

diagnostic studies for shock

Answer 32

• Thorough history and physical examination
• No single study to determine shock
  
  • Blood studies
    
    • Elevation of lactate
    • Base deficit
  • 12-lead ECG
  • Chest x-ray
  • Hemodynamic monitoring

Question 33

successful management of shock includes

Answer 33

• Identification of patients at risk for shock
• Integration of patient’s history, physical examination, and clinical findings to establish diagnosis
• Interventions to control or eliminate cause of dec perfusion
• Protection of target and distal organs from dysfunction
• Provision of multisystem supportive care

Question 34

Management strategies of shock general

Answer 34

• General management strategies
  
  • Ensure patent airway.
  • Maximize oxygen delivery (sat above 90%)
• Cornerstone of therapy for septic, hypovolemic, and anaphylactic shock = Volume expansion
  
  • Isotonic crystalloids (e.g., normal saline) for initial resuscitation of shock
  • 2-3 liters fluid, then give a blood produc
• Volume expansion
  
  • If patient does not respond to 2 to 3 L of crystalloids, blood administration & central venous monitoring may be instituted.
    
    • Complications of fluid resuscitation: Hypothermia & Coagulopathy

Question 35

primary goal of drug therapy in shock

Answer 35

Primary goal of drug therapy = Correction of decreased tissue perfusion

• Vasopressor drugs (e.g., norepinephrine)
  
  • Achieve/maintain MAP >60 to 65 mm Hg.
  • Reserved for patients unresponsive to fluid resuscitation
• Vasodilator therapy (e.g., nitroglycerin, nitroprusside)
  
  • Achieve/maintain MAP >65 mm Hg.

Question 36

nutrition in shock care

Answer 36

Nutrition is vital to decreasing morbidity from shock.

• Initiate enteral nutrition within the first 24 hours.
• Initiate parenteral nutrition if enteral feedings contraindicated or fail to meet at least 80% of caloric requirements
• Monitor protein, nitrogen balance, BUN, glucose, electrolytes
• Need high calories/protein

Question 37

collaborative care cardiogenic shock

Answer 37

• Restore blood flow to myocardium by restoring balance between O2 supply and demand.
• Thrombolytic therapy
• Angioplasty with stenting
• Emergency revascularization
• Valve replacement
• Hemodynamic monitoring
• Drug therapy (e.g., diuretics to reduce preload)
• Circulatory assist devices (e.g., intraaortic balloon pump, ventricular assist device)
• to decrease contractility: beta blockers

Question 38

hypovolemic shock collaborative care

Answer 38

• Management focuses on stopping loss of fluid and restoring circulating volume.
• Fluid replacement is calculated using a 3:1 rule (3 mL of isotonic crystalloid for every 1 mL of estimated blood loss).
• may need a vasopressor if this isn’t working

Question 39

collaborative care septic shock

Answer 39

• Fluid replacement to restore perfusion
  
  • Hemodynamic monitoring
• Vasopressor drug therapy
• Vasopressin for patients refractory to vasopressor therapy
• IV corticosteroids for patients who require vasopressor therapy, despite fluid resuscitation, to maintain adequate BP
• Antibiotics after cultures obtained (e.g., blood, wound exudate, urine, stool, sputum)
• Drotrecogin alfa (Xigris)-Major side effect: bleeding
• Glucose levels <150 mg/dL (combination of tpn and nutrition)
• Stress ulcer prophylaxis with histamine (H2)-receptor blockers
• Deep vein thrombosis prophylaxis with low-dose unfractionated heparin or low-molecular-weight heparin

Question 40

pt. with neurogenic shockIn spinal cord injury: spinal stability

Answer 40

In spinal cord injury: spinal stability

• Treatment of hypotension and bradycardia with vasopressors and atropine
• *Fluids used cautiously as hypotension generally is not related to fluid loss
• Monitor for hypothermia (warming blankets)

Question 41

general treatment for anaphylactic

Answer 41

• Epinephrine, diphenhydramine
• Maintaining patent airway
  
  • Nebulized bronchodilators
  • Endotracheal intubation or cricothyroidotomy may be necessary.
• Aggressive fluid replacement
• Intravenous corticosteroids if significant hypotension persists after 1 to 2 hours of aggressive

Question 42

obstructive shock general care

Answer 42

• Early recognition and treatment is primary strategy.
• Mechanical decompression
• Radiation or removal of mass
• Decompressive laparotomy

Question 43

nursing assessment in shock

Answer 43

• ABCs: airway, breathing, and circulation
• Focused assessment of tissue perfusion
  
  • Vital signs
  • Peripheral pulses
  • Level of consciousness
  • Capillary refill
  • Skin (e.g., temperature, color, moisture)
  • Urine output
• Brief history
  
  • Events leading to shock
  • Onset and duration of symptoms
• Details of care received before hospitalization
• Allergies
• Vaccinations

Question 44

nursing diagnosis

Answer 44

• Ineffective tissue perfusion: renal, cerebral, cardiopulmonary, GI, hepatic, and peripheral
• Fear
• Potential complication: organ ischemia/dysfunction

Planning

Goals for patient

• Assurance of adequate tissue perfusion
• Restoration of normal or baseline BP
• Return/recovery of organ function
• Avoidance of complications from prolonged states of hypo-perfusion

Question 45

nursing implementation

Answer 45

Health promotion

• Identify patients at risk.
  
  • Elderly patients
  • Those with debilitating illness
  • Those who are immunocompromised
  • Surgical or accidental trauma patients
• Planning to prevent shock
  
  • Monitoring fluid balance to prevent hypovolemic shock
  • Maintenance of hand washing to prevent spread of infection

Acute interventions

• Monitor the patient’s ongoing physical and emotional status to detect subtle changes in the patient’s condition.
• Plan and implement nursing interventions and therapy.
• Evaluate the patient’s response to therapy.
• Provide emotional support to patient and family.
• Collaborate with other members of health team when warranted.

Neurologic status: orientation and level of consciousness

Cardiac status

• Continuous ECG
• VS, capillary refill
• Hemodynamic parameters: central venous pressure, PA pressures, CO, PAWP
• Heart sounds: murmurs, S3, S4
• Respiratory status

Respiratory rate and rhythm

• Breath sounds
• Continuous pulse oximetry
• Arterial blood gases
• Most patients will be intubated and mechanically ventilated.
• Urine output
• Tympanic or pulmonary arterial temperature
• Skin: temperature, pallor, flushing, cyanosis, diaphoresis, piloerection
• Bowel sounds
• Nasogastric drainage/stools for occult blood
• I&O, fluid and electrolyte balance
• Oral care/hygiene based on O2 requirements
• Passive/active range of motion

Assess level of anxiety and fear.

• Medication PRN
• Talk to patient
• Visit from clergy
• Family involvement
• Comfort measures
• Privacy
• Call light within reach

Question 46

nursing evaluation

Answer 46

• Normal or baseline, ECG, BP, CVP, and PAWP
• Normal temperature
• Warm, dry skin
• Urinary output >0.5 mL/kg/hr
• Normal RR and SaO2 ≥90%
• Verbalization of fears, anxiety

Question 47

When assessing a patient in shock, the nurse recognizes that the hemodynamics of shock include:

1. Normal cardiac output in cardiogenic shock.
2. Increase in central venous pressure in hypovolemic shock.
3. Increase in systemic vascular resistance in all types of shock.
4. Variations in cardiac output and decreased systemic vascular resistance in septic shock.

Answer 47

4. Variations in cardiac output and decreased systemic vascular resistance in septic shock.

Question 48

The nurse determines that the patient in shock has progressed beyond the compensated stage when laboratory tests reveal:

1. Increased blood glucose levels.
2. Increased serum sodium levels.
3. Increased serum potassium levels.
4. Increased serum calcium levels.

Answer 48

3. Increased serum potassium levels.

Question 49

• 26-year-old man arrives via paramedics to ED with multiple gun shot wounds to abdomen.
• Unresponsive, BP 58/30, HR 146
• Three units type O packed RBC given for profuse blood loss before surgery
• Surgery successful in removing bullets and repairing blood vessels
• Surgeon estimated he lost at least
  3 L of blood before surgery and 1 L more during surgery.He is admitted to ICU.

1. What complications will you anticipate with this amount of blood loss?
2. What fluids can you expect to administer?
3. What medications will likely be ordered?
4. What should you monitor hourly or every 2 hr?

Answer 49

1. hypovolemic shock
2. Administer LR, PRBCS, NS
3. Give levofed
4. Monitor LOC, Cardiac Monitor/tele

Question 50

Ideal Qualities for a Biologic Terrorist Agent

Answer 50

• High rate of illness among those exposed
  
  • High attack rate
• High rate of death among those who get ill
  
  • High case fatality rate
• Short time between onset of illness and death
  
  • Small window to start treatment
• Low level of immunity in the population
• No effective or available treatment
• Can be transmitted person to person
• Easy to produce and disseminate
• Difficult to diagnosis either clinically or diagnostically (i.e. laboratory identification)

Question 51

Priority Biological Agents

Answer 51

Bacterial

• Anthrax
• Plague
• Tularemia
• Brucellosis
• Q fever
• Other
  
  • food borne pathogens
  • waterborne pathogens

Viral

• Smallpox
• Viral Hemorrhagic Fevers
• Viral Encephalitis

Toxins

• Botulism
• Staph Enterotoxin B
• Ricin toxin
• Tricothecene mycotoxins

Question 52

Anthrax

Answer 52

• Gram positive spore forming bacterium Bacillus anthracis
• Primarily disease of herbivores which are infected by ingesting spores in soil
• Natural transmission to humans by contact with infected animals or contaminated animal products
  
  • “Woolsorter’s disease”
• Three forms of disease
  
  • Cutaneous
  • Inhalational
  • Gastrointestinal (GI)

Question 53

Epidemiology and transmission of anthrax

Answer 53

direct contact, ingestion (lesion), and inhalation

Question 54

cutaneous anthrax

Answer 54

• Accounts for 80% of naturally occurring Anthrax cases
• Enters through openings in skin from abrasions, lacerations
• 20% progress to systemic form if untreated
• Most cases recover

Question 55

anthrax inhalation

Answer 55

• Inhalation of spores
• Incubation, 2-3 days (range up to 60 days)
• Spores engulfed by macrophages and transported to mediastinal and peribronchial lymph nodes
• Insidious onset: malaise, low grade fever, nonproductive cough
• Abrupt development of respiratory distress
• Hemorrhagic mediastinitis
• Hematogenous spread
• Meningitis in 50%, usually fatal

Question 56

pt. care of inhalation anthrax

Answer 56

Ciprofloxacin

• 400 mg intravenous every 12 hours for adults
• 10 -15 mg/kg intravenous every 12 hours for children

Doxycycline

• 100 mg intravenous every 12 hours for adults and children > 8 yr and > 45 kg
• 2.2mg/kg every 12 hours for children
• < 8 yr (up to 200 mg/day)

*IDEALLY USE BOTH

PLUS

• One or two additional anti-microbial agents effective against anthrax (e.g. imipenem, clindamycin, rifampin, macrolides)

Additional issues

• Penicillin should never be used as a monotherapy
• If meningitis is suspected, an antibiotic with good CSF penetration should also be administered (e.g. rifampin or chloramphenicol)
• Supportive therapy for shock, fluid volume deficit and airway management may be needed.
• Drainage of pleural effusions may improve clinical outcome

Anthrax Immune Globulin (AIG) can be used to neutralize anthrax toxin.

Question 57

Anthrax: Post-Exposure Prophylaxis

Answer 57

Start 60 days of oral antibiotics ASAP after exposure

• Ciprofloxacin or Levofloxacin

OR

• Doxycycline

OR

• Amoxicillin or Penicillin (if known PCN sensitive)

Vaccine: Can be given post-exposure in conjunction with antibiotics

Question 58

Smallpox

Answer 58

• Variola virus, two forms of the disease: minor and major
• Spread via respiratory droplets or aerosols expelled from the oropharynx
• May also spread via direct contact
• Patients are most contagious during the time at which the skin rash is present
• Approx. 30% of patients exposed go on to develop the disease
• Approx. 30% mortality with ordinary smallpox

Question 59

smallpox characteristics

Answer 59

• Febrile Syndrome – occurring 1-4 days prior to rash.
• Classic Smallpox lesion – deep-seated, firm/hard, round, well-circumscribed; lesion may become umbilicated or confluent.
  
  • Can be mistaken chicken-pox
• Febrile Syndrome – occurring 1-4 days prior to rash.
• Lesion in Same Stage of Development – Evolve from macules → papules → pustules at the same time.
• Centrifugal distribution – First lesion on oral mucosa, face, or forearms.
• lesions on palms and soles

Question 60

smallpox vs. Chickenpox distribution

Answer 60

Spares the trunk: Smallpox

Primarily the trunk: chickenpox

Question 61

clinical timeline for smallopox

Answer 61

• exposure
• incubation period: 12 days (range 7-19 days)NOT Infectious
• Prodrome phase (2 - 4 days): Abrupt onset of fever >38.3°C, Malaise/myalgia, Headache, Nausea/vomiting, Backache,
  Usually NOT Infectious
• Early Rash Phase: Mucous membrane lesions. Small red spots on the tongue and throat. Lesions enlarge, ulcerate, then shed virus. Infectious 24 hours before visible skin rash
• Rash Phase: (21 days) macules, papules, vesicles, pustules, scabs, Infectious until all scabs fall off

Question 62

Smallpox: Medical Management

Answer 62

• Strict respiratory/contact isolation of patient
  
  • Patient infectious until all scabs have separated
• Treatment is supportive care only
• Antivirals are under evaluation
  
  • Cidofovir
  • ST246

Question 63

Smallpox: Prevention and Control

Answer 63

• Immediate vaccination of ALL close contacts (< 6 ft) and ALL contacts of patients contacts (Ring vaccination)
• Vaccination within 4 days of exposure may prevent or lessen disease
• Mass vaccination may be necessary and/or everyone may want to be vaccinated

Question 64

Smallpox current vaccine

Answer 64

• Live vaccinia virus
• Because it is a live virus, there can be adverse events from vaccination
  
  • Occurs mostly in immunologically suppressed persons
• Immunity is not life-long, but having been vaccinated in the past may reduce morbidity and mortality

Question 65

Plague and types

Answer 65

• Plague is a severe bacterial disease of humans and animals produced by the gram negative nonsporulating bacillus Yersinia pestis
• Bite of a rodent flea that is carrying the plague bacterium, or by handling an infected animal
• Hundreds of millions of people died
• when human dwellings were inhabited
• by flea-infested rats
• Modern antibiotics are effective, but without prompt treatment the disease can likely cause illness or death

Types:

• Bubonic
• Septicemic
• Pneumonic

Question 66

plague epidemiology and natural transmission

Answer 66

Routes of Plague Transmission

Animal Resovior

A = Bite of Flea
B = Contact with animal or carcass
C = Inhalation of respiratory droplets
D = Contact with sputum or fluid

Question 67

Clinical Presentation of Pneumonic Plague

Answer 67

*exposure

*IncubationPeriod: 1-6 days

*Early Presentation: Abrupt onset of fever, malaise, headache, myalgia, Chest pain and dyspnea, Tachypnea (particularly in young children), Productive cough (sputum may be purulent or watery, frothy, blood-tinged), Hemoptysis

*Antibiotic therapy in the first 24 hours can prevent septicemia, cardio-respiratory failure, shock, and death

*Late Presentation

• Rapid progression to pulmonary disease/ARDS
• Pulmonary edema, dyspnea, cyanosis
• Meningitis may be a complication
• Hypotension, DIC, septicemia, and death
• Lab findings – bacterial infection and sepsis
• Organism usually seen on sputum gram stain
• Mortality approaches 100% if untreated in 24 hours

Question 68

Plague: Patient Care

Answer 68

Early antibiotic treatment* is paramount to patient survival

Adults:

• Streptomycin 1 gm IM b.i.d. for 10 days (DRUG OF CHOICE);
• Chloramphenicol 25 mg/kg IM or IV 4 times daily for 10 days
• Gentamicin 5 mg/kg IM or IV once daily for 10 days;
• Doxycycline 100 mg IV b.i.d. or 200 mg IV once daily for 10 days;
• Ciprofloxacin 400 mg IV b.i.d. for 10 days;

Children:

• Streptomycin 15 mg/kg IM twice daily for 10 days (max 2 gm/day);
• Chloramphenicol 25 mg/kg IV 4 times daily for 10 days (max 4 gm/day)
• Gentamicin 2.5 mg/kg IM or IV 3 times daily for 10 days;
• Doxycycline 2.2 mg/kg IV twice daily for 10 days (max dose 200mg/day);
• Ciprofloxacin 15 mg/kg IV twice daily for 10 days (max 1 gm/day)

*CDC recommends initiating treatment with two drugs believed effective against Y. pestis until antimicrobial susceptibility data is available on isolates.

Question 69

Plague: Prophylaxis

Answer 69

• Pneumonic plague contacts (transmitted via droplets)
  
  • Oral Doxycycline or Ciprofloxacin
  • For 7 days after last exposure
• Vaccine no longer manufactured

Question 70

Botulism

Answer 70

Caused by toxin from Clostridium botulinum

• Colorless, odorless and tasteless
• Lethal dose for 70kg human is 1ng/kg
  
  • Botulinum toxin is the most lethal neurotoxin known to man
  • Dispersal of aerosolized toxin, 1 gm of aerosolized toxin could kill up to 1.5 million people

Question 71

botulism epidemiology and natural transmission

Answer 71

• C. botulinum in the soil, flora and fauna (in honey and botox)
• Toxin production in foods prepared or stored at ambient temperature
• Colonization and toxin production in an open wound
• Intestinal colonization and toxin production in susceptible infants and adults
• Botulism:Acute, symmetric, descending flaccid paralysis with bulbar palsies

Question 72

clinical presentation of botulism

Answer 72

exposure

I_ncubation Period_:

• Inhalational: 24-72 hours
• Foodborne: 18-36 hours (range 2 hours to 8 days) Dependent on toxin dose

Cranial Nerve Palsies: Cranial Nerves III, IV, VI, VII, IX

• Blurry vision
• Diplopia
• Ptosis
• Expressionless Facies
• Regurgitation
• Dysarthria/Dysphagia

Descending Flaccid Paralysis: Symmetric Paralysis
Voluntary Muscles

1. Neck
2. Shoulders
3. Upper extremities
4. Lower extremities

*BP often normal; Mental status normal

Question 73

Botulism: Medical Management

Answer 73

• Early administration of antitoxin: within 24 hours, 1 vial per person, acts by binding to free toxins in the system
• Supportive care
  
  • Monitoring respiratory function
  • Providing mechanical ventilation
  • May be needed for weeks or months

Question 74

Viral Hemorrhagic Fevers (VHF)

Answer 74

Hemorrhagic fever viruses (RNA) belong to four taxonomic families:

• Filoviridae (Ebola/Marburg)
• Arenaviridae (Bolivian HF))
• Bunyaviridae (Congo-Crimean HF)
• Flaviviridae (Dengue)

Natural vectors – virus dependent

• Rodents, mosquitoes, ticks

No natural occurrences in U.S.

Question 75

VHF as a Biological Weapon

Answer 75

These viruses are considered suitable weapons because:

• they have a low infectious dose
• they cause high morbidity and mortality
• they cause fear and panic in the general public
• effective vaccines are either not available, or supplies are limited

Question 76

Clinical timeline for VHF

Answer 76

exposure

incubation period:

• 2-21 days (depending on the virus)

Early Manifestations

• High fever
• Headache
• Myalgia
• Arthralgia
• Anorexia
• Varying degrees of nausea, vomiting and diarrhea

Later Manifestations

• External and internal hemmorage
  
  • Ecchymosis
  • Petechiae
  • Bleeding from puncture site
  • Bleeding from nose and gums
  • Hemorrhagic conjunctivitis
  • Gastrointestinal bleeding
  • Severe vaginal bleeding
  • Pleural effusion
  • Renal Failure
  • Shock
• Laboratory Findings
  
  • Leukopenia or leukocytosis
  • Thrombocytopenia
  • Elevated Liver Function Tests
  • Anemia or Hemoconcentration
  • Prolonged PT, PTT

Question 77

VHF Clinical Management

Answer 77

• Aggressive supportive care with intravenous fluids, colloids, blood products as needed
• Specific therapy (ribavirin) may be helpful in bunyaviruses and arenaviruses
• Avoid IM injections or invasive procedures (due to bleeding)
• Strict aerosol precautions (i.e. respiratory isolation)