ADVANCED TOPICS 2010 – CBI Case 1
Title: 56 y.o.woman with progressive weakness
Chief Complaint:
Joan Marshall is a 56 year old nurse who presents to the Emergency Department at UMC on April 13,
2012 at 1010 hours with a history of chills, lightheadedness, and weakness over the past 24 hours.
Pre-session Activity: (released Friday @ 3 pm)
Provide two hypotheses with rationales for this patient’s condition.
1.
2.
3.
4.
5.
Infection/Sepsis
Anemia
Malignancy
Drug RxN
Dehydration




Dizziness
Orthostasis
X NVD + Melena
SOB
HPI
PMHx
 MVA w/FX
 Splenectomy
SocialHx
 + Smoking
 X EtOH
Initial Physical Exam
 BP 72/41
 P123
 RR 34
 39.1 C
 97% O2 Sat
Secondary Physical Exam
 40.5 C
 P 128
 RR 20
 BP 98/50 After 2LNS + NE
Labs
 Leukopenia
 NML Hb and HCT
 Thrombocytopenia (DIC)
 Left Shift
 Howell-Jolly bodies (asplenism)
 Mild pulmonary edema
 Metabolic Acidosis
 Elevated BUN/Creatinine (prerenal)
 Elevated Lactate (decreased perfusion)
 Increased PT & PTT (DIC)
 + strep pneumoniae
Learning Issues
1. Howell-Jolly Bodies
2. Acid-Base Balance
3. Labs: Bun/Creatinine, PT, PTT, INR
4. Presentation and Primary Evaluation of
Shock
5. 4 Types of Shock and pathogenesis
6. Shock treatment
7. Blood Gasses + O2 sat machine
Friday Session: Presentations
Acid/Base Basics:

CO2 + H20H2CO3HCO3 + H

Metabolic Acidosis: Low pH, HCO3, PCO2. Caused by production of H (shifts equation to the left) with compensatory
hyperventilation and buffering by HCO3.
o Sx. Fatigue, SOB, abdominal pain, kussmaul resp, HTN, tachypnea.
o MUDPILES (Anion Gap): Methanol, urea, diabetic ketoacidosis, paraldehyde, Fe, lactate, ethanol,
salicylates (Aspirin).

Respiratory Acidosis: Low pH, high HCO3 & PCO2. Caused by retention of CO2 (shifts eqtn to the right).

Metabolic Alkalosis: High Ph, HCO3, and PCO2. Caused by loss of H ions (shifts equation to the right) with
compensatory hypoventilation.
o Sx: Apathy, stupor, confusion, tetani.

Respiratory Alkalosis: High pH, HCO3, low PCO2. Caused by hyperventilation (shifts equation to the left).
PT, PTT, TT, Bun:Creatinine:

PT: (WEPT: Warfarin-extrinsic-PT or Martin’s Lucky7 pEt) Prothrombin time. Measures extrinsic (7) and central (10, 5,
2, 1) pathway and warfarin activity. Vitamin K dependent pathway.

PTT: Partial thromboplastin time. Measures intrinsic (12, 11, 9, 8) and central (10, 5, 2 thrombin, 1 fibrin) pathway and
heparin activity.

TT: Thrombin time. Measures conversion of fibrinogen to fibrintime to clot.

Creatinine: Breakdown product of creatine in muscle. Filtered + secreted by the kidney so serum concentration =
urine concentration (Serum Cr)(Blood Vol)=(Urine Cr)(Urine Vol)

BUN: Urea levels in the blood.

Ratios:
o >20:1Prerenal
o 10-20:1Normal Kidney
o <10:1Intrarenal
Clinical Presentation and Evaluation of Shock:

Sx:
o Flushed and
o Cool clammy
o Hyperventilatio
Warm/Sepsis
skin
n
o Hypotension
o AMS
o Tachycardia
o Oliguria
o Metabolic
o Prolonged cap
acidosis
refill

Evaluation:
o H&P + ECG + CXR
o Labs: CBC, BUN/CR, Chem Panel, Cardiac Enzymes, ABG’s, Toxicology Screens, Urinalysis
o MGMT: Airway support (to intubate or not), breathing (ventilation, CPR, O2), circulation (blood loss,
vascular collapse, thrombosis, etc).
Pathogenesis of Shock

Shock: Multisystem organ hypoperfusion. Can be compensated (normal BP) or decompensated (low BP).

Types: Hypovolemic (volume loss), cardiogenic (heart failure), neurogenic (vasodilation/bradycardia due to nervous
alteration), septic.

Pressure/Volume: BP=SVR x CO
o SVR=Systemic vascular resistance
o CO=HR x SV
o SV=EDV-ESV

Septic Shock:
o Mechanism: Cytokine storm, decreased arterial resistance due to elevated NO, decreased venous tone,
toxins, pulmonary dysfunction, etc. All our body’s response to the overwhelming infection.
Splenic Function/Dysfunction
 Function:
o Secondary lymphoid organ
o Filters blood to remove bacteria & old RBC’s
o Sequesters platelets
o Stores FE
o Site of extramedullary hematopoesis
 Splenomegaly: Occurs when RBC’s get stuck in the sinusoids and congest the spleen (ie spherocytosis, SS
Dz), an immune response is occurring, liver failure/CHF cause vascular congestion, metabolic diseases,
malignancy.
 Asplenism: Increased susceptibility to encapsulated organisms. Marker: Howell-Jolly bodies (left-over
DNA from nuclear expulsion).
Shock Treatment
 Identification: Thorough H & P, gram stain,
 Early Management:
o Stabilization of airway: Intubation, mechanical ventilation, chest radiographs, ABG’s
o Assess perfusion: Blood pressure and clinical evidence (cyanosis, cool clammy skin, restlessness,
oliguria, lactic acidosis)
o Fluids/Meds/Monitoring/Infusions: Central venous catheter
o We want to reach 70% oxygen tension and CVP 8-12
o Volume infusion in the presence of septic shock is indicated, 500mL IV isotonic saline infusion
bolus.
o Pressors: NE, dopamine, vasopressin
o Additional Therapies: Treat the underlying cause (in sepsis: IV antibiotics, removal of infected
catheters, debridement/amputation, abscess draining)
o Constant monitoring is important!
Learning Objectives:
Differentiate among types of shock.
 Shock: Global hypoperfusion affecting all major body systems.
o Cardiogenic: Associated with heart problems (not able to pump enough blood)
o Hypovolemic: Associated with low blood volume (not enough blood to pump)
o Distributed: Associated with widespread vasodilation (think SHOCK)
o Neurogenic: Associated with dysfunction of neural control (widespread vasodilation, loss of
cardiac control, baroreceptor defects, etc)
o Anaphylactic: Result of severe allergic reaction (due to histamine release by mast cells)
o Obstructive: Due to obstruction of blood flow (cardiac tamponade, tension pneumothorax, PE)
Define sepsis and septic shock.
 Sepsis: Overwhelming disseminated bacterial/fungal/viral (uncommon) infection with widespread
inflammation. Usually caused by a gram - organism (E.coli, klebsiella, proteus that produce endotoxin), or
by a toxin producing gram + organism (streptococcus/staphylococcus).
 Septic Shock: Life threatening drop in blood pressure caused by overwhelming sepsis. Two things must be
present to diagnose septic shock: systemic infection + refractory hypotension. The hypotension is caused by
a combination of our body’s immune response to insult (cytokine release) and the offending agent’s
pathologic mechanisms (toxins, LPS, tissue necrosis, etc) causing widespread vasodilation. This leads to
end organ hypoperfusion causing lactic acidosis, renal failure (w/oliguria), and altered mental status.
Identify the physiologic disturbances that underlie septic shock and the key components of resuscitation for
these disturbances.
 Vasodilation: A result of both the body’s release of cytokines and the organism’s release of toxins/antigens.
This is corrected by infusing isotonic saline and using vasopressors such as norepinephrine to raise blood
pressure.
 DIC: Endothelial/platelet activation + tissue damageHypercoagulable state with formation of
microthrombi which consume platelets and coagulation cascade factors and leave the body vulnerable to
bleeds (if DIC is severe).
 End organ hypoperfusion: Direct result of vasodilation, corrected by restoring vascular tone and/or blood
volume.
 Lactic acidemia: End organ hypoperfusion forces tissues to utilize anaerobic metabolism as a means of
producing ATP. The product of anaerobic metabolism is lactate, which builds up in the blood and causes
an acidemia.
 Tachypnea: Occurs not only as an attempt to compensate for decreased organ perfusion, but also to correct
lactic acidemia.
 Kidney Failure: A result of both end organ hypoperfusion and DIC.
-Initial - During this stage, the hypoperfusional state causes hypoxia, leading to the mitochondria being unable to produce
adenosine triphosphate (ATP). Due to this lack of oxygen, the cell membranes become damaged, they become leaky to extracellular fluid, and the cells perform anaerobic respiration. This causes a build-up of lactic and pyruvic acid which results in
systemic metabolic acidosis. The process of removing these compounds from the cells by the liver requires oxygen, which is
absent.
-Compensatory (Compensating) - This stage is characterized by the body employing physiological mechanisms, including neural,
hormonal and bio-chemical mechanisms in an attempt to reverse the condition. As a result of the acidosis, the person will begin
to hyperventilate in order to rid the body of carbon dioxide (CO2). CO2 indirectly acts to acidify the blood and by removing it the
body is attempting to raise the pH of the blood. The baroreceptors in the arteries detect the resulting hypotension, and cause the
release of adrenaline and noradrenaline. Noradrenaline causes predominately vasoconstriction with a mild increase in heart rate,
whereas adrenaline predominately causes an increase in heart rate with a small effect on the vascular tone; the combined effect
results in an increase in blood pressure. This is known as Cushing reflex and its triad is the subjective identifying characteristic of
this stage. Renin-angiotensin axis is activated and arginine vasopressin (Anti-diuretic hormone; ADH) is released to conserve
fluid via the kidneys. Also, these hormones cause the vasoconstriction of the kidneys, gastrointestinal tract, and other organs to
divert blood to the heart, lungs and brain. The lack of blood to the renal system causes the characteristic low urine production.
However the effects of the Renin-angiotensin axis take time and are of little importance to the immediate homeostatic mediation
of shock
-Progressive (Decompensating) - Should the cause of the crisis not be successfully treated, the shock will proceed to the
progressive stage and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, sodium ions build
up within while potassium ions leak out. As anaerobic metabolism continues, increasing the body's metabolic acidosis, the
arteriolar smooth muscle and precapillary sphincters relax such that blood remains in the capillaries. Due to this, the hydrostatic
pressure will increase and, combined with histamine release, this will lead to leakage of fluid and protein into the surrounding
tissues. As this fluid is lost, the blood concentration and viscosity increase, causing sludging of the micro-circulation. The
prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion. If the bowel becomes
sufficiently ischemic, bacteria may enter the blood stream, resulting in the increased complication of endotoxic shock.
-Refractory (Irreversible) - At this stage, the vital organs have failed and the shock can no longer be reversed. Brain damage and
cell death have occurred. Death will occur imminently.
Treatment consists of:

Stabilization of airway: Intubation, mechanical ventilation, chest xray, ABG’s

Fluids/Meds/Monitoring/Infusions: Central venous catheter

Want to reach 70% central venous oxygen saturation and CVP 8-12 mmHg

Volume infusion with 500mL IV isotonic saline bolus.

Vasopressors: NE, dopamine, vasopressin

IV Antibiotics
Define the health risks for splenectomized patients or those with impaired splenic function.
 Individuals without a spleen are at an increased risk for development of severe encapsulated bacterial
infections (S. pneumoniae, Haemophilus influenzae, N. Gonorrhea). Platelet count may be abnormally
high because the spleen acts to sequester platelets until they are needed.