Leg pain, chest and back pain, shock CIS (Darrow) Flashcards

1
Q

A 55 year old man is seen for progressive bilateral leg and calf pain
with ambulation and relief with sitting down in a chair. History is
positive for hypertension and the patient is on an ACE inhibitor.
Physical examination reveals an S4 (atrial contraction into a non-compliant ventricle- can be caused by DM and HTN). Present BP is 130/60. He has a
“simian gait” (duck walk) and complains of worse pain with extension of his
back and improvement with bending forward. Calves are tender.
Pedal pulses are questionably diminished. Which test will most
likely be positive?

Ankle/brachial index
Femoral angiography
Lumbar spine xray
Lumbar MRI
Venous doppler
A

Lumbar MRI

so spinal stenosis can look like PAD ***

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2
Q

A 45 y/o diabetic presents with burning, dorsal foot pain that is relieved by getting up or dangling the foot (gravity pulls blood into the foot). How do you know this is not diabetic neuropathy? How is the diagnosis made? What is the treatment?

A

tibial and pedal artery occlusion

DM neuropathy- not relieved with gravity-hanging leg

Diagnose by MRA

Treatment: Vein bypass to distal tibial or pedal arteries.

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3
Q

A 35 y/o male from south Africa presents with sudden onset PAIN in the right lower extremity. The leg is PALE, WEAK, and NUMB (DONT see dependent rubor). The pedal pulses are absent and the foot is cold. The heart rhythm is irregular What has happened?

A

acute arterial occlusion of a limb

a-fib potentially- and most likely had a clot?

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4
Q

which is true regarding the acute arterial occlusion of a limb

A. 50% of cardiac emboli go to the brain.
B. With loss of light touch, surgery can be deferred.
C. Before revascularization, NaCl should be administered.
D. Cause is never due to thrombosis.
E. Pedal pulse are not palpable.

A

Answer E. Pedal pulse are not palpable.

Which is true in regard to the above?
A. 50% of cardiac emboli go to the brain. no go to legs
B. With loss of light touch, surgery can be deferred. surgery should be done immediately
C. Before revascularization, NaCl should be administered NO, bicarb should be administered, get rid of lactic acid
D. Cause is never due to thrombosis No

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5
Q

what are the 6 p’s of arterial occlusion

A
Pain 
Pallor
Paralysis
Paresthesias
Pulselessness
Poikilothermia*- irregular
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6
Q

A 58 y/o hypertensive, diabetic, female presents with dizziness, diploplia, dysphagia, dysarthria, dysmetria, and ataxia of 50 minutes duration. The patient is having which type of an event?

A. Vertebro-basilar TIA
B. Carotid stroke
C. Brain tumor symptoms
D. Seizure disorder
E. Diabetic neuropathy 

know the D’s!!

A

A - vertebro-basilar TIA

have carotid system in front and vertebral basilar system in the back.

This patient is presenting with the D’s of VB TIA”S

Dizziness
Diplopia
Dysphagia
Dysarthria 
Dysmetria
Duration
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7
Q

Define carotid territory TIA… (3 things)

A

unilateral weakness or numbness on one side of body

aphasia

amaurosis fugax - transient vison loss

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8
Q

A 45 y/o hyperlipidemic, diabetic female has had abdominal pain lasting for 2 hours after meals for the past 3 years. She has had a 20 lb weight loss over the past 6 months related to fear of eating. She presents suddenly with periumbilical pain, but no significant clinical abdominal findings except for bloating. The patient has a (an):

mesenteric occlusion.
ruptured appendix.
diabetic neuropathy.
pancreatic cancer.
inflammatory bowel syndrome.
A

**mesenteric occlusion.

not tender, not really bloated, but they have severe pain and this is an emergency!! - they can get a bowel infarction very quickly

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9
Q

what is the treatment for mesenteric occlusion

A

Angioplasty and stent versus aorto-celiac or superior mesenteric bypass

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10
Q

A 65 y/o female with a history of polycythemia and frequent phlebotomies presents with abdominal pain and swelling. Two months ago she had an episode of amaurosis fugax (carotid pathology) and two weeks ago, she had left sided numbness that lasted for 10 minutes (TIA) . She has been having abdominal pain after meals (abdominal angina) for the past 6 months. Hb is 18 gm with (polycythemic) WBC of 13,000 and platelets of 350,000 (Increased). Exam shows abdominal enlargement with dullness to percussion in the flanks. A CT angiogram is performed and shows portal vein thrombosis. What is most unusual in this patient?

Amaurosis fugax
Abdominal enlargement
Polycythemia
Portal vein thrombosis
Left sided numbness
A

she is having problems in both the arterial and venous systems***

Portal vein thrombosis

JAK 2 disease

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11
Q

what is a red clot

A

Caused by multiple thrombophilic* and /or
Hypofibrinolytic** factors, mostly inherited. Also
due to acquired risk factors (pregnancy, BCPs,
high dose steroids, immobilization, surgery,
and foreign bodies in the blood stream/catheters

anything that causes stasis/ coagulation cascade activation

mostly venous clotting

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12
Q

white clot causes?

A

due to platelet aggregation

Caused by smoking,
hypertension, hyperlipidemia,
DM, cholesterol emboli. (atherosclerotic causes)

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13
Q

what causes venous AND arterial clotting

A

Heparin induced thrombocytopenia (HIT) (patient on heparin gets a clot)

Paroxysmal Nocturnal Hemoglobinuria (PNH)

Myeloproliferative disease (especially JAK 2)–>

Anti Phospholipid Antibody Syndrome (APLAS)

Anti Cardiolipin Antibody Syndrome (ACLA)

Hyperhomocysteinemia

Thromboangitis obliterans
(Buerger’s disease: vasculitis of arteries and veins).

Nephrotic syndrome (antithrombin III, protein S and C deficiency).

Right to left shunt

Popliteal artery aneurysm

Know in general ==> HIT and Jak2

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14
Q

what is the treatment for an aortic aneurysm …

what is a significant aneurysm size… and what are they usually associated with?

A

Treatment–>
Labetolol 20 mg over 2 min IV, then 40 -80 mg q 10 min
Esmolol 0.5 mg/kg IV
Nitroprusside 50 mg in 1000 D5 at 0.5 mL/min
Surgical repair or endovascular graft

Truly significant aneurysm is 5-6 cm… and usually associated with coronary artery disease

BEFORE you repair this, make sure to repair the coronary arteries b/c they probably have CAD - so put in a stent in or something

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15
Q

A tall, thin 35 y/o male presents for a flight physical to renew his license for Delta. During the exam he is found to have a 3/6 diastolic decresendo murmur (aortic insufficiency) at the base, with a 2/6 systolic murmur at the apex that lengthens with standing and shortens with handgrip (mitral valve–> mitral insufficiency). History is positive for a prior pneumothorax. Which would be an additional finding in this patient?

Posterior mid-thoracic machinery-murmur
Aortic root dilation
Pulseless left arm
Hoarseness
Paraplegia
A

***aortic root dilation - he has Marfan’s

Murmurs:
Hand grip (increase afterload)- should be louder, but in this case it wasn’t it was weaker!! This is not standard mitral regurg
With standing –> it lengthens/louder in this patient – less blood is filling usually with standing, and this murmur should quiet DOWN but It didn’t. so this is not standard mitral regurg

this is mitral valve prolapse (which is NOT standard mitral regurg) - this is typically seen in Marfan syndrome

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16
Q

Which is associated with a dissecting aortic aneurysm?

Dissection into the adventia
Dull aching chest pain 
Anterior wall MI
Systolic murmur
Hypertension
Paraplegia 

what else can you see dissection in?

A

HTN and paraplegia

paraplegia- in 4% of people the vessels to the spinal cord come off the descending aorta!

it is dissecting into the media

Can also see dissection in pregnancy, bicuspid aortic valve (problems with aortic root), and coarctation.

–sharp tearing chest pain NOT Dull

– doesn’t give anterior wall MI –> inferior wall MI*** b/c the right coronary artery comes off next to the aortic valve

–Doesn’t give you a systolic murmur, it gives you a diastolic murmur- Aortic insufficiency ***

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17
Q

Know the symptoms of a dissecting ascending thoracic aortic aneurysm
versus a descending thoracic aortic aneurysm as given in Lange’s CMDT!

A

know it

ascending–> chest pain, sudden onset, radiating down back or into neck
a diastolic murmur may develop as a result of the dissection in the ascending aorta close to the aortic valve, causing valvular regurg, heart failure and tamponade

descending
syncope, hemiplagia, or paralysis of the lower extremities, peripheral pulses may be diminished or unequal

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18
Q

what is the medical treatment for an expanding or dissecting aortic aneursm…

A

surgery

or graft

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19
Q

what else produces mediastinal widening ?

A

Artifact – patient rotated. Chest X-ray is rotated and gives you pseudo-widening

Mediastinal Mass – T and B cell lymphoma, teratoma, thyroid, thymus = 4 Ts

Vessels – aortic aneurysm

Anthrax

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20
Q

peripheral artery aneurysm ….

presentations

A

An easily palpable popliteal pulse*** may well be an aneurysm which can present with loss of distal pulse with acute leg or foot pain

Popliteal aneurysms account for 70% of peripheral arterial aneurysms – risk include thrombosis and embolization.

In treatment, surgery is indicated for peripheral embolization, > 2cm *** or a mural thrombus.

Often can be conservative if light touch remains in tact.- if they can’t feel light touch this prompts IMMEDIATE surgery

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21
Q

Which of the following predisposes to thrombophlebitis?

Tachycardia
Exercise
NSAIDs
Vitamin E
Trauma
A

Trauma

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22
Q

what is virchow’s triad

A

Hypercoagulability
Stasis
Trauma

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23
Q

A 59 y/o male with pancreatic cancer presents with a two week history of a swollen left leg with calf tenderness. Physical exam shows a superficial phlebitis of the left arm. The cause of these findings is most likely:

systemic hypercoagulability.
Staphylococcus superinfection.
pressure related to the pancreatic mass.
related to IV catheters.
related to chemotherapy.
A

systemic hypercoagulability.

every patient with cancer is prone to clots–> trousseau’s syndrome

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24
Q

what is trousseau’s syndrome

A

Armand Trousseau who diagnosed himself with gastric cancer.

 Involves mucin (glycans) producing epithelial cancers that activate platelet and leukocyte (P and L) selectins*** (CD62/glycoproteins or cell adhesion molecules/CAMs) that lead to platelet rich microthrombi *** (seen most often in adenocarcinoma of the lung).
activation of platelets !!

whenever you have cancer you have hypercoaguable state

Thrombogenic cancers: gastric, esophageal, lung, pancreas, renal, ovarian, AML, non-Hodgkins lymphoma*.

if there is cancer, there is increased risk for clots - due to P and L selectins

cancers are sticky*** and that’s why metastases occurs

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25
Q

Bernard soulier

A

GpIb deficiency

results in bleeding

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26
Q

Glanzmann thrombasthenia

A

GpIIb-IIIa deficiency

results in bleeding

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27
Q

72 year old male with traumatic ulcer on his ankle?

A

venous insufficiency

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28
Q

venous ulcers….

A
History of trauma***, pregnancy, and varicose veins
Medial malleolus*** is usually medial 
Superficial, irregular margins***
Ruddy, beefy***, fibrinous,  granulation
Edema
Dermatitis
Lipodermatosclerosis –indurated*** 
Hyperpigmentation***
Moderate to heavy exudate***
Cap refilling - < 3 sec (Normal)
ABI = 0.9 or greater normal
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29
Q

arterial ulcers

A

History of smoking, rest pain claudication*
Site of pressure

Deep, “punched out” with sharp borders*
Bed pale grey or yellow
*
Dry * necrotic base with eschar
Lateral
Pale, hair loss, cold feet, atrophic skin, no pulses
*
Cap filling >4-5 sec
ABI = 0.5 or less (not normal)

30
Q

neuropathic ulcers?

A

diabetics

History of numbness
Common in DM***
Pressure site
Variable depth
Surrounding callus*** (hard)
Cap refilling normal
ABI = normal

*Diabetic foot infections: more likely with positive probe to bone test, ulcer duration > 30 days, trauma , PVD, peripheral neuropathy, and RI.

31
Q

septic superficial thrombophlebitis

treatment?

A

red streaks - usually occurs near IV insertion site

Vancomycin 15 mg/kg IV q 12 hrs
Ceftriaxone 1 gm IV q 24 hrs

32
Q

Phlegmasia Cerulean (blue) Dolens*

what is this due to?
causes?

A

Literally inflammatory (edematous), blue, and painful, ie. painful, sky blue and inflamed!

Due to primary venous insufficiency (leg can’t drain and it swells and then causes blockage of arteries) with secondary arterial
insufficiency *** (not so in AF where emboli cause primary arterial occlusion and pallor occurs).

** Most common cause is cancer, though may be obesity, old age, immobilization, or other procoagulant conditions (Factor V Leiden, etc) .

BLUE cyanotic

swells up so much that it blocks the arteries–> can lose limb

can present in hypovolemic shock b/c there is so much fluid in the leg

make sure to check the patient for cancer

33
Q

treatment of Phlegmasia cerulean dolens ?

A
  1. Fluid
  2. Anticoagulation
  3. Evaluate for cancer***
34
Q
A 64 y/o male with lung cancer presents with dizziness, blurred vision and headache. Physical exam shows flushed facies and dilated neck veins. This patient has developed:
A. mets to the brain.
B. CVA.
C. vena cava obstruction.
D. pulmonary embolus.
E. pneumonia.  

Which type of lung cancer would this be?

A

C. vena cava obstruction

Non small cell lung cancer is the most common cause of the vena cava syndrome* followed by small cell and then lymphoma . Pancoasts syndrome is more often due to NSCLC as well, especially squamous and adenocarcinoma

at night - face is swollen

35
Q

What else causes SVC obstruction?

A

Cancer

Chronic fibrotic mediastinitis (reaction to Histoplasmosis antigen) --> fibrosis, can block off the vena cava

 DVT from arm veins

 Aortic arch aneurysm

 Constrictive pericarditis
36
Q

A 35 y/o black female presents with malaise, anorexia, sweating, chills, fever and throbbing pain in the left arm. There is warmth at the left antecubital fossa and a faint red streak is discovered over the dorsal left hand. The left axillary nodes are swollen. She denies any bites. The most appropriate question would be as to whether or not she has a:

cat.
horse.
dog.
parrot. 
Ferret.
A

Cat- this is classic scratch fever - Bartonella henselae

cat licks its paws- from the saliva

  • Bartonella henselae (cat scratch fever)
  • Pasturella multicodia
  • Capnocytophagia (usually from dog bites) - DF2
37
Q

lymphedema

what is characteristic?

A

there are NO ulcers***
massive swelling

Lymphedema = pitting edema without ulcers, varicose veins or stasis pigmentation

Milroy’s

Stewart-Treves syndrome –

38
Q

what is Milroy’s

A

Milroy’s disease 1892 – (described in a missionary from India)

– congenital lymphedema with break in the VEGFR 3 gene (the gene controls lymphogenesis)

problem with the vascular epithelial growth factor receptor so you get agenesis of lymphatics

39
Q

what is Stewart-Treves syndrome

A

actually a hemangiosarcoma rather than a lymphangiosarcoma due to local immunodeficiency (possibly radiation contributes)

seen in patients who have had their breast removed. chronic lymphadema develops into hemangiosarcoma

40
Q

what is the definition of shock?

A

Arterial blood flow inadequate to meet tissue needs for O2.

Tissue perfusion depends on CO and SVR with

CO depending on preload, contractility and afterload
and

SVR depending on viscosity, vessel length and diameter, ie SVR = vL/r4.

shock can be defined by***
preload
CO
afterload

41
Q

hypovolemic shock

A

– decreased CO and PCWP (CVP < 5 mmHg) with increased SVR ***

  1. Hemorrhage induced  
  2. Fluid loss induced
  3. Poor intake
42
Q

Cardiogenic shock

A

– decreased CO*** (< 2.2 l/min) with increased PCWP (pulmonary capillary wedge pressure-left atrium) and SVR (systemic vascular resistance)

  1. Cardiomyopathies  
  2. Arrhythmias     
  3. Mechanical  
  4. Extracardiac /Obstruction 
         (tension pneumothorax, PE, 
          cardiac tamponade)
43
Q

what is distributive shock

A

Distributive
(vasodilatory - “warm shock” ) –

increased CO*** b/c there is no afterload (> 4.0 L/min/m2) with decreased SVR (< 800 dynes.S/cm-5) and decreased PCWP (can be normal) as seen in sepsis, toxic shock syndrome, anaphylaxis, toxin reactions (heavy metal, insect bites, etc.), spinal cord injury (neurogenic), myxedema, or adrenal crisis.

May also have normal (70%) to high*** central venous O2 saturation (CVOS) due to redistribution of flow.

all the blood is going to the skin! - skin doesn’t take up alot of oxygen so this is why the CVOS is normal b/c the oxygen is not being utilized by the skin where all the blood is

44
Q

Clinical shock markers

what are the 3 windows of the body?

A
  1. Systolic BP < 90 mm Hg (or mean BP < 60-65 mm Hg)
  2. The 3 windows of the body:
    Cutaneous - mottled extremities, livedo reticularis

Renal - 1.0 mmol/L

45
Q

A 56 year old alcoholic patient with cirrhosis and ascites presents with vomiting, dry mucous membranes, clammy skin, oliguria, mental status change and BP of 70/50. This patient has which type of shock?
Large distended abdomen

Hypovolemic
Cardiogenic
Distributive
Septic
Obstructive
A

This patients vascular volume–> is all in the abdomen. So this patient is hypovolemic b/c the fluid is not in the vascular tree

Hypovolemic
He is not making protein normally

46
Q

A 56 year old alcoholic patient with cirrhosis and ascites presents with vomiting, dry mucous membranes, clammy skin, oliguria, mental status change and BP of 70/50. Which parameter will be found?
A. Decreased CVP (normal 0-5 mmHg)
B. Increased CO (normal 2-4 L/min/m2)
C. Increased PCWP (normal 4-12 mmHg)
D. Decreased SVR (normal 800-1500 dyne-sec-cm-5)

A

Decreased CVP (normal is 0-5) - b/c there is low blood volume, its all in his abdomen

NOT PCWP- b/c this will be decreased (normal is 4-12 mmHg)

CO will be normal/low (normal is 2-4 L/min)

47
Q

treatment for hypovolemic shock?

A

hypovolemic shock is CVP < 5 mm Hg

Tx:
1. 0.9% saline – 1-2 liters wide open – continue based on BP, skin, urine and mentation.

  1. PRBCs
    - give blood if very low

Goal to obtain CVP 8-12 mmHg

48
Q

A 52 y/o female diabetic presents with dyspnea and BP of 65/50. History is positive for an old MI. The patient is on a loop diuretic, an aldosterone antagonist, an ACE inhibitor, and a beta blocker. Heart rate is 140. The skin is cool and clammy and the patient is restless. There are bilateral basilar crackles and the neck veins are distended. This patient most likely has which type of shock?

Hypovolemic
Cardiogenic
Distributive
Septic
Obstructive
A

Cardiogenic ***

–>* CVP > 18 mm Hg and Cardiac Index

49
Q

how would you treat cardiogenic shock?

A

1 Upright, O2, NIPPV

  1. Low BP – dobutamine (initial 0.5-1 mcg/kg/min with maintainamce of 2-20 mcg/kg/min) or milrinone with intraaortic balloon counterpulsation

Use NE if its cardiogenic due to MI**
Use dobutamine if its cardiogenic NOT due to MI **

  1. Normal or high BP – IV nitroglycerin or nitroprusside with IV loop diuretic (furesomide)
  2. AF – esmolol or cardioversion
  3. Post MI – antiplatelets, norepinephrine* or dopamine if hypotensive (dobutamine or milrinone# for those with vasoconstriction and not as severe hypotension)
  4. IABP, CABG, or PCI
50
Q

A 46 y/o female with lung cancer presents with dyspnea and cough. Heart sounds are distant and lungs are clear. Neck veins are distended. BP is 60/40. EKG is shown.

This patient has (a)(an):

CHF.
cardiomyopathy.
myocardial infarction.
pericardial tamponade.
ventricular septal rupture. 

see EKG–> the heart is swinging back and forth …. electrical alterans

A

pericardial tamponade

“Bag of water” around the heart

preload is way up

51
Q

what is beck’s triad for cardiac tamponade? ***

A

Distended neck veins

Distant heart sounds (muffled)

Distressed BP (Hypotension)

52
Q

TEE shows an echo free space anterior and posterior to the left ventricular wall. This represents which type of shock?

A

cardiogenic–> but obstructive !

heart can’t fill normally

53
Q

what are other causes of obstructive shock?

A
Tension pneumothorax
Pericardial disease
Disease of pulmonary circulation (PE)
Cardiac tumor (myxoma)
Left atrial mural thrombus
Obstructive valvular disease
54
Q

A 25 y/o HIV patient presents with cough, fever of 39 C and heart rate of 98 beat/min. Respiratory rate is 26 breaths/min with WBC of 9,000 cells/mm3 with 15% bands (bandemia) Glucose is 145 mg/dL. This patient most likely has:

Systemic Immune Response Syndrome.
sepsis.
severe sepsis.
pancreatitis.
vasculitis 

What is the usual acid base imbalance at this stage?

A

SIRS

has respiratory alkalosis*** which is the FIRST thing that develops in SIRS

breathing very fast–> low PCO2 and high pH

2nd thing that happens is–> moves to lactic acidosis

LABS:
CMP
ABG's
Type and crossmatch
Coagulation parameters
Blood cultures
Lactate
55
Q

what is SIRS

What labs should be ordered?

A

systemic immune response syndrome

  • fever
  • increased HR
  • increased RR
  • high white blood cell count (12,000)
  • bandemia

can go on to sepsis
sepsis can go on to shock

Dysregulated inflammation related to autoimmune disorders, pancreatitis, vasculitis, VTE, burns, surgery, etc.
Same category as sepsis.

56
Q

what labs do you obtain in SIRS, sepsis, or distributive shock?

A
CBC
CMP
ABGs
Type and crossmatch
Coagulation parameters
Lactate
Blood cultures
57
Q

A 25 y/o HIV patient presents with cough, fever of 39 C and heart rate of 98 beat/min. Respiratory rate is 26 breaths/min with WBC of 9,000 cells/mm3 with 15% bands (bandemia) Glucose is 145 mg/dL. This patient most likely has SIRS

A gram stain sputum is obtained on the above patient and shows clusters of a gram positive cocci. One may now diagnose:

A. SIRS
B. sepsis
C. septic shock
D. severe sepsis 
E. refractory septic shock
A

gram positive- staph pneumonia

he now has B. SEPSIS b/c we have proof of a bug

which is related to Pathogen-Associated Molecular Patterns (PAMPs), ie. glycolipids, glycoproteins, lipoproteins, peptidoglycans, lipopolysaccharides, mannoproteins, DNA, RNA, etc. which activate Pattern Recognition Receptors*** (Toll-like receptors) to release cytokines and chemokines and thus produce SIRS/Sepsis.

DAMPS’s (own cells releasing things) and PAMPS- activate your receptors on macrophages –> you release IL-1, IL-6, IL-8, TNF alpha, interferon gamma–> SEPSIS AND DEATH

58
Q

Findings in Sepsis/SIRS

A
Infection plus: 
General variables 
TPR changes –T > 38.3C or < 36C; HR > 90 bpm; RR > 20bpm
Glucose > 140 mg/dL
Altered mentation
Edema of > 20mL/kg over 24 hours
59
Q

inflammatory variables of Sepsis

A

WBC > 12,000 with bandemia > 10%; WBC < 4,000

Increased CRP and procalcitonin (increased CD 64)

60
Q

hemodynamic variables in sepsis

A

SBP* < 90 mmHg;

MAP < 70 mmHg

worsens with development of sepsis

61
Q

what occurs later in sepsis?

organ dysfunction variables?

A

PaO2/FiO2 < 300 ( 0.5 mg/dL (> 2 mg/dL)

urine output 0.5

INR > 1.5 or PTT > 60 seconds

Ileus

Platelets < 100,000 microl-1

Bilirubin > 4 mg/dL-

Hyperprolactinemia > 1 mmol/L (tissue hypoxia)

Decreased capillary refill (tissue hypoxia)

62
Q

SIRS to sepsis to severe sepsis

How do you diagnose severe sepsis ?

A

significant dysfunction in just ONE organ

Most common evidence of severe organ dysfunction are ARDS, ARF and DIC; or serum
lactate > 4 mmol/L.

63
Q

The above patient is considered to have developed septic shock when unable to maintain a mean arterial pressure > 60 mmHg after:

activated protein C.
fluid resuscitation. 
calcium channel blockers.
sodium bicarbonate.
antibiotics.
A

Fluid resusication

this is the definition of septic shock

64
Q

Distributive shock, including septic shock, anaphylaxis, or adrenal insufficiency is characterized by:
A. decreased CO.
B. increased PCWP.
C. SVR

A

decreased afterload, systemic vascular resistance is low

SVR

65
Q

how do we treat septic shock

9 steps ?

A

9 steps to be done within 2 hours for patients with infection, SIRS, and dysfunction of one organ.

Serum lactate
Two sets of blood cultures
Two 18 gauge lines
Start antibiotics
Give 2 liters NS
CBC and BMP
O2 sat > 90%
Start norepinephrine if shock is present.
Transfer for lactate > 4 mmol/L, Systolic BP < 90 mm Hg, or MAP < 60 after 2 liters of NS.
66
Q

what is early goal directed therapy ?

CVP
MAP
Central venous O2 sats?
Lactate levels?

A
  1. Need to maintain CVP at 8-12 mm Hg. Fluids*** 5 liters in initial 6 hrs.
  2. Need to maintain MAP at > 65 mm Hg and cardiac index at 2-4 liters/min2. Vasopressors . Use Norepinephrine initial 1-2 mcg/min IV with maintainance of 2-4 mcg/min. May use phenylephrine for warm shock. Epinephrine for anaphylactic shock at 1 mcg/min. Vasopressin 0.01-0.04 units/min (potentiates norepinephrine. Possible benefit of norepinephrine, vasopressin ,steroid combo).
  3. Need to maintain central venous O2 saturation at > 70%.* For < 70% give PRBC* to obtain hemacrit of 30%. If still < 70%, then dobutamine* as ionotropic therapy.
  4. Hope to reduce lactate by 20% in first 2 hours. (Increased glycolysis, inhibition of pyruvate dehydrogenase, and impaired liver function, all increase lactate levels)
67
Q

steroids and septic shock?

A

Cortisol response of 9 ug/dL or less after 250 mcg of ACTH =

relative adrenal insufficiency – use hydrocortisone 50 mg q 6 hrs.

68
Q

A 60 y/o diabetic male presents with cramping pain in both calves with walking 2-4 blocks. The femoral arterial pulses seem somewhat diminished in the groin, the left popliteal and left pedal pulses are diminished. The right pedal pulses are absent. The Ankle/Brachial index is 0.5 on the left and 0.1 on the right. There is no hair on the right toes and the patient has dependent rubor on the right. The patient most likely has severe occlusion of the:

  1. In the above patient, under what conditions would it have been possible to have a more normal ABI on the right (ie .8 or .9) and still have poor circulation?
  2. What is Osler’s sign or maneuver?
A

superficial femoral

If the profundus femoral were involved, the
claudication would occur much earlier

  1. When the vessels are calcified* as in diabetics. This does not allow
    practical use of ABI and thus one must resort to wave form analysis.
  2. Oslers Pseudohypertension because
    of calcified vessels. Have to pump the cuff way up to occlude the vessel
69
Q

how would you treat a patient with occlusion of the superficial femoral artery…

A

treatment of superficial, common femoral and popliteal stenosis is femoral-popliteal bypass

70
Q

how does lateral medullary syndrome present?

A

with occlusion
of vertebral or PICA = ringing in the right ear, dizziness and
right facial pain. There is nystagmus on right lateral gaze.
There is right perceptive deafness. Intention tremor is present
on the right with falling to the right with Romberg position.
There is loss of pain and temperature over the right face
and opposite trunk and extremities with ptosis of the right eye
and constriction of the right pupil..