Detailed presentation of a patient in shock with scientific discussion

1. Case presentation
on Management
of Shock
Moderator- Dr Wondimu (Internist)
Dr Fasika (MD)
Prepared by - Dr Michael S (MI)

2. Outline
- Case Presentation
- Definition
- Type
- Stages
- Diagnosis
- Management

3. IDENTIFICATION
Name –F.E
Age-30 Sex- M
Address-SORO
Date of admission-Tahisas 16, 2012EC
Date of discharge-Thaisas 18, 2012EC

4. C/C- Referred from primary hospital
• HPI
A 30 year old male patient referred from primary hospital with diagnosis of hypovolemic
shock 2ry to GI loss after he presented with complain of diarrhea & vomiting of 4 day
duration. The vomiting is non bilious, non projectile containing ingested matter and the
diarrhea is profuse and watery . Associated with headache and altered mentation. For
this reason he went to primary hospital and was resuscitated with 4 bags of fluid & took
ceftriaxone 1gm iv
otherwise
-no hx abm
-no hx fever
-no hx DM.HTN,

5. PHYSICAL EXAMINATION
GENERAL APPERANCE- ASL
VITAL SIGNs- BP- unrecordable RR- 40 T- 37.1
PR-120 Feeble RBS- 32mg/dl
HEENT -pink conjunctiva, non icteric sclera
Chest - Rales on the lower 1/3rd of post chest bilaterally
CVS - S1 & S2 well heard. No murmur or organo megally
ABD- flat, non palpable organo megally
GUS- catether insitu, has UO
MSS/INT- no rash/edema
CNS=GCS-11/15 (E4V2M5)
pupil midsized & sluggishly reactive bilaterally

6. ASSESSMENT- SEPTIC SHOCK(GI focus) + hypoglycemia
PLAN
ADMIT TO ICU
Put on face mask
CBC,ESR,PICT,VIRALMARKER,CXR,U/A,OFT, RBS Q1HR
Resuscitate with 1 bag of NS
Start Ceftazidime 2g IV TID & Vancomycine 1g IV TID
Start Dopamine with 5mcg/kg/min, 2 vials in 500ml start with 5 drops/min
RBS Q1hr

7. INVESTIGATION
CBC (16-4-12)
WBC-2,400
L-19.6% G-68.8%
RBC-3.46
HGB-11.1
HCT-31.1
PTL-129
HBSAg and Anti HCV Ab- negative

8. PROGRESS NOTE @ ICU 16-4-12
P- SEPTIC SHOCK 2ry ? GI ONSET SEPSIS + HYPOGLYCEMIA + ? MENINIGITIS
HX
 DIARRHEA and
VOMITING of 4 days
 ALTERED MENTATION
OF 1 DAY
PE
GA-ASL
V/S PR-120 FEEBLE BP-UNRECORDABLE
RR 36 T 37.1
HEENT-PINK CONJUCTIVA, NIS
RS-TRANSMIIT SOUND ALL OVER LUNG
CVS- S1& S2 WELL HEARD
ABD- FLAT & NO PALPABLE ORGANO MEGALLY
GUS- NO CVAT UO- 1L OVER 12HRS
MSS/INT- NO EDEMA/RASH
CNS-
GCS-13/15(E4V4M5)
PUPIL MIDSIZED& SLUGISH
MOVES ALL EXTRIMITIES
NUCHAL RIGIDITY +VE
PLAN
 40% GLUCOSE BOLUS
 Mf WITH 40% ADDED
 CIMETIDINE MAINTENANCE
 DEXAMETHASONE 8MG IV QID
 CEFTAZIDIME& VANCOMYCINE
 START DOPAMINE WITH 5MCG
AND ESCALATE UNTIL BP
MENTAINE Q1HR
 COLLECT INVX

10. PROGRESS NOTE @ ICU 17-4-12
P-SEPTIC SHOCK 2ry GI ONSET SEPSIS + CORRECTED HYPOGLYCEMIA+ ASPIRATION PNEUMONIA+
P.MENIGITIS
HX
 HIGH GRADE
FEVER
 ALTERRED
MENTATION
PE
 GA-ASL
 V/S- PR 82 FEEBLE BP-69/43
RR-24 T- 38.6 SPO2- 945 w O2
 HEENT-PINK CONJUCT, NIS
 RS-COARSE CREPTATION ALL OVER
LUNG
 CVS-S1&S2 WELL HEARD
 ABD-NO ORGANOMEGALLY
 GUS-CATHETER IN SITU
 MSS/INT-NO RASH/EDEMA
 CNS
GCS9/15(E3V2M4)
PUPIL MIDSIZED & REACTIVE
NORMOTONIC
NECK STIFFNESS- +VE
PLAN
 CONTINUE SAME MAGT
 ADD METRENDAZOLE 500 MG IV TID
 PCM 1gmQID
 CIMETIDINE 200MG IV BID
 UFH 5000 IU SC BID

11. INVESTIGATIONS
17-4-12
WBC-17,000 RBC-4.52
G-96.9 HGB -13.7
L-2.3 HCT-39.6
PTL- 113,000
CSF ANALYSIS(17-4-12)
PROTEIN- 0.1 mg/dl
GLUCOSE-44 mg/dl
LDH-6765
Gram stain-
GRAM –VE COCCI SEEN
OFT(17-4-12)
UREA-31
CR-1.19
ALP-140
SGOT-203 SGPT-83
BF- No H/P seen (2x)

12. PROGRESS NOTE @ ICU 18-4-12
P= Increased ICP + Coma 2ry P. Meningitis + Septic Shock (GI focus) + Aspirn Pneumo + Deteriorating
HX
 HIGH GRADE FEVER
 LOC
PE
 GA-ASL
 V/S- PR 42 FEEBLE BP-87/61 RR-34
T- 36.5 SPO2-69-70 ON FACE MASK
 HEENT-PINK CONJUCTIVA, NIS
 RS-COARSE CREPTATION ALL OVER LUNG
 CVS-S1&S2 WELL HEARD
 ABD-NO ORGANOMEGALLY
 GUS-CATHETER INSITU UOP-450ML/6HR
 MSS/INT-NO RASH/EDEMA
 CNS
GCS-6/15(E2V1M3)
PUPIL DIALATED & SLUGGISH
NORMOTONIC
NECK RIGIDITY +VE
PLAN
 CONTINUE SAME MANGT
 HEAD ELEVATION TO 15 DEG
 MANITOL 2G/ KG IV
 CONSIDER MRI(UNAFFORDABLE)

13. On 18-4-12 patient left against medical advice
after his attendants signed an AMA form.

14. Definition
• Shock is a physiologic state characterized by a significant reduction of
systemic tissue perfusion resulting in decreased oxygen delivery to the
tissues
• Creates an imbalance between oxygen delivery and oxygen
consumption
• Prolonged oxygen deprivation leads to cellular hypoxia and
derangement of critical biochemical processes at the cellular level
which can progress to the systemic level

15. • Shock based on the type in general has a high mortality rate ranging
from 20-80%
• The early phase of these shocks is reversible and the aim of treatment
is to prevent irreversible cellular damage and restore normal function
of the circulatory system

16. Normal tissue perfusion
• Determined by Mean Arterial Pressure (MAP)
MAP = Cardiac Output x Systemic Vascular Resistance
HR Stroke Volume
Contractility
Afterload
Preload

17. Types of Shock
I. Hypovolemic
II. Cardiogenic
III. Obstructive
IV. Distributive

18. Hypovolemic Shock
- Decreased Intravascular volume (Preload) with a properly .
. functioning heart leading to a decreased Stroke Volume
Causes (either loss of blood or loss of body fluid)
- Hemorrhage - trauma, GI bleed, AAA rupture or ectopic pregnancy
- Loss of fluid - burns, GI losses, dehydration, third spacing (e.g.
pancreatitis, bowel obstruction) or DKA

20. Cardiogenic Shock
- Shock where the heart is unable to pump adequate amount of blood that will
lead to inadequate perfusion of organ and tissue
Causes
Decreased Contractility
MI, myocarditis, cardiomyopathy or Post resuscitation syndrome following
cardiac arrest
Mechanical Dysfunction
Papillary muscle rupture post-MI, Severe Aortic Stenosis or Rupture of
ventricular aneurysms
Arrhythmia
Heart block, VT, SVT or atrial fibrillation
Cardiotoxic drugs
B-blocker & Calcium channel blocker OD

21. Obstructive Shock
Shock in a patient with a properly working heart with obstruction to
the return or outflow tract of the heart
Causes (either an obstructed return or outflow tract)
Outflow obstructions
• Massive pulmonary embolism
• Aortic dissection
• Cardiac tamponade
• Tension pneumothorax
Venous return obstruction
• Vena cava syndrome - eg.
neoplasms, granulomatous
disease

22. Distributive Shock
Shock where heart functions properly but the preload is severely decreased
secondary to peripheral vasodilation (loss of vessel tone)
Inflammatory loss of vessel tone
Septic shock
Anaphylactic shock
Post resuscitation syndrome following cardiac arrest
Decreased sympathetic nervous system function
Neurogenic - cervical or upper thoracic spinal injuries
Toxins
Drug overdose (a1 antagonists)

23. Type of Shock Problem Problem results in Body Compensation
Hypovolemic Heart pumps well, but not
enough blood volume to
pump
↓CO
↓Preload
↑SVR
Cardiogenic Heart fails to pump blood
out
↓CO
↓Contractility
(depending on the cause)
↑SVR
Obstructive Heart pumps well, but the
outflow is obstructed
↓CO
↓Preload or
↑Afterload
(depending on the cause)
↑SVR
Distributive Heart pumps well, but there
is peripheral vasodilation
↓SVR
↓Pre load
↑CO

24. Stages of Shock (Despite the type of shock)
Progression will depend on:
- Patient (age, comorbidities,Immunity)
- Cause
- Intervention
Insult
Preshock
(Compensation)
Shock
(Compensation failed)
End organ
Damage
Death

25. Diagnosis Based on History, Physical Examination and Investigations
On History
- Anxiety
- Agitation
- Confusion, delirium & coma
- Fever
- Diarrhea, vomiting or loss of appetite
- Polyuria
- Hemorrhage
- Chest or epigastric pain
- Palpitation
- Trauma to the back
- History of drug use

26. On PE
-Tachycardiya HR > 100
With fast febile thready distal pulses
Rhythm irregularity
Few exceptions are
- Patient with neurogenic shock
- HR of > 90 is considered tachycardia in an athlete who usually have a lower resting
heart rate (called relative tachycardia)
- Bradycardic causes of shock like a heart block

27. - Tachypnea RR> 20
which will be shallow, irregular and labored
- Blood pressure
In pre-shock stage it will be normal
Systolic < 90 mmHg OR MAP < 65 mmHg
40 mmHg drop in systolic BP from the baseline (relative .
. hypotension)

28. -HEENT- Dry tongue and buccal mucosa
-Respiratory System
Cyanosis, asymmetric chest movement, use of accessory muscles
Tenderness, shifted trachea, altered tactile fremitus
Decreased or absent breath sound

29. - Cardiovascular System
Diminished peripheral pulses
Distended neck veins with elevated JVP
Quiet precordium (MI), shifted AI (cardiomyopathy)
Shifted PMI (cardiomyopathy)
Distant heart sound (Tamponade), Murmurs (Post MI, aortic
. stenosis)

30. -Integumentary
Cold & clammy (Cardiogenic, Obstructive & Hemorrhagic)
Warm (Distributive shock)
Dry Axilla
- Low Urine output of <0.5 ml/kg/hr

31. Diagnostic criteria
- Ill appearance or altered mental status
- Heart rate >100
- Respiratory rate > 22 (or PaCO2 < 32 mmHg)
- Urine output < 0.5 ml/kg/hr
- Arterial hypotension for more than 20 minutes
- Lactate > 4
Presence of 4 out of 6 of the above criteria will diagnose shock

32. Management
- Shock management begins with ABC of life
- Airway should be kept patent and protections should be applied if the
patinet can’t protect the airway
- Intubation if
Unabel to oxygenate
Unabel to maintain airway
To decrease work of breathing (which increases O2 consumption
. by 50-100% and decrease cerebral blood flow by 50%)

33. Breathing
- Assesed for causes of hypovolemic shock (massive hemothorax), obstructive
shock (cardiac tamponade, tension pneumothorax)
- Patient put on oxygen
Circulation
- Assesed for active bleeding or fluid loss
- Central or peripheral large bore IV access
- Management starts with Fluid resuscitation but following steps depend on
type of shock

34. Hypovolemic shock
- Management aimed at replacing the lost blood or fluid
- Replacement is either with a colloid or a crystalloid
- Establish 2 large bore IV or central line
- Infusion of fluid (Normal saline or Ringer lactate) 1 L over 20–30
minutes fast and additional 1-2 L over the following 1-2 hrs

35. Reassess the patient for adequacy of treatment by following
Mental Status
HR, RR and BP
Capillary refill
Skin turgor
Dryness of buccal mucosa
Urine output
If needed repeat the bolus with maximum tolerated dose being 60 – 80 ml/kg with
in the first 1 – 2 hr.
If shock persists consider ongoing blood/ fluid loss or septic shock

36. - If Hgb< 7 transfuse of PRBC or whole blood 20ml/kg
over 4 hrs
- Hct should be kept below 35
- Repeat as needed until Hgb level reaches 10gm/dL
- Type-specific or O-negative blood can be used
- Following severe &/or prolonged hypovolemia,
inotropic support with NE, vasopressin or dopamine
may be required but only after blood volume has been
restored

37. Cardiogenic Shock
Treatment aimed at managing the underlying cause
- Lasix for fluid overload
- Atrial Fibrillation: Cardioversion or Rate control
- Inotropes - Dobutamine +/- Norepinephrine
(Vasopressor)
- Look for precipitating causes

38. Treatment of acute MI
- In addition to the usual treatment of acute MI initial
therapy is aimed at maintaining adequate systemic
and coronary perfusion by raising systemic BP with
vasopressors
- Adjusting volume status to a level that ensures
optimum LV filling pressure.

39. - Hypoxemia & acidosis must be corrected and
most pts require ventilatory support
- Negative inotropic agents should be discontinued
- Hyperglycemia should be controlled with insulin.
- Bradyarrhythmias may require transvenous
pacing.
- Recurrent ventricular tachycardia or rapid AF
may require immediate intervention

40. Vasopressors
- used to augment BP and cardiac output in patients with
cardiogenic shock
- Norepinephrine is a potent vasoconstrictor and
inotropic stimulant that is useful for patients with
cardiogenic shock.
- As first line of therapy norepinephrine was associated
with fewer adverse events, including arrhythmias,
compared to a dopamine randomized trial of patients

41. Distributive shock
- Septic shock management
- Sepsis no longer defined as SIRS + suspected or proven
infection
- Now defined as suspected or proven infection + acute
increase of > 2 SOFA (Sequential Organ Failure
Assessment) score points

43. Septic shock
- Previously defined as Sepsis + Refractory Hypotension with
Systolic BP <90 mm Hg or 40mm Hg drop from baseline BP
Mean arterial pressure <65 mm Hg
Unresponsive to fluid challenge (20-40mL/kg)
- Now defined as Sepsis + Vasopressor therapy needed to elevate and
keep MAP > 65mmHg and Lactate >2 mmol/L (18 mg/dL) despite
adequate fluid resuscitation

45. The ‘Feast’ Trial

46. - Successful management requires urgent measures to
treat the infection, to provide hemodynamic and
respiratory support & to remove or drain infected
tissues.
- These measures should be initiated within 1 h of the
patient’s presentation with severe sepsis or septic
shock.

47. - Ventilator therapy is indicated for progressive hypoxemia,
hypercapnia, neurologic deterioration or respiratory muscle
failure.
- Sustained tachypnea (respiratory rate, >30 breaths/min)
- Mechanical ventilation is often initiated to ensure adequate
oxygenation, to divert blood from the muscles of respiration,
to prevent aspiration of oropharyngeal contents, and to
reduce the cardiac afterload

48. - The primary goals are to restore adequate oxygen and
substrate delivery to the tissues as quickly as possible and to
improve tissue oxygen utilization and cellular metabolism.
- Adequate organ perfusion is essential.
- Circulatory adequacy is assessed by measurement of arterial
blood pressure and monitoring of parameters such as
mentation, urine output and capillary refill
- Initial management of hypotension should include the
administration of IV fluids, typically beginning with 1–2 L of
normal saline over 1–2 h.

49. - The urine output rate should be kept at >0.5 mL/kg per
hour by continuing fluid administration
- a diuretic such as furosemide may be used if needed.

50. Vasopressor
- Vasopressor administration is required for persistent hypotension once
adequate intravascular volume expansion has been achieved
- The goal of vasopressor therapy is to reverse the vasodilation and
altered blood flow distribution

51. Norepinephrine
• The first line for septic shock
• It has predominant alpha receptor agonist and potent peripheral
vasoconstrictor with out significant increment of HR or cardiac output
• Dose range 5-20 microgram/min
• Norepinephrine preferred over dopamine because dopamine has unfavorable
arrhythmia and elevation in pulmonary capillary wedge pressure (PCWP).

52. - Dopamine
• Has varying effect depending on dose
• Low dose (<5 mic gm/kg /min)
much effect on B- receptor ( increase cardiac contractility & HR)
• High dose (5-10 mic gm/kg /min)
much effect on alpha – receptor ( result vasoconstriction)
• Dopamine is useful in setting of cold shock (vasoconstriction exists) and
cardiac output is too low to maintain tissue perfusion

53. - Second line agent for pt who has persistent hypotension despite
maximum dose of norepinephrine and dopamine
• Epinephrine
• phenylephrine
• vasopressin
- Epinephrine
• increase MAP mainly by inotropic effect
• Considered in pt with poor response for NE. and DOP.

54. Antibiotics
- Antimicrobial chemotherapy should be started as soon as samples of blood and
other relevant sites have been obtained for culture.
- Treat empirically then change when culture result comes back
- Initiate empirical antimicrobial therapy that is effective against both gram-
positive and gram-negative bacteria
- The chosen antimicrobial regimen should be reconsidered daily in order to
provide maximal efficacy with minimal resistance, toxicity, and cost

55. - Most patients require antimicrobial therapy for at least 1 week.
- The duration of treatment is typically influenced by factors such as
• the site of tissue infection,
• the adequacy of surgical drainage,
• the patient’s underlying disease, and
• the antimicrobial susceptibility of the microbial isolate(s)

56. - If Pseudomonas is unlikely pathogen, favor combining vancomycin
with one of the following
• 3rd generation Cephalosporin (ceftriaxone or cefotaxime) or
• Beta lactam inhibitor (piperacillin-tazobactam , ticarcillin-clavulanate)
OR
• Carbapenem (imipenem or meropenem )

57. - If Pseudomonas is a possible pathogen, favor combining vancomycin with
two of the following
• cephalosporin ( ceftazidime , cefepime ), or
• carbapenem (imipenem, meropenem ), or
• beta-lactam inhibitor (piperacillin-tazobactam , ticarcillin-clavulanate ), or
• Fluoroquinolone (ciprofloxacin ), or
• Aminoglycoside ( gentamicin , amikacin ), or
• Monobactam ( aztreonam )
- Selection of two agents from the same class should be avoided

58. - Removal or drainage of a focal source of infection
- Sites of occult infection should be sought carefully, particularly in the
lungs, abdomen, and urinary tract.
- Indwelling IV or arterial catheters should be removed and the tip rolled
over a blood agar plate for quantitative culture;
- after antibiotic therapy has been initiated, a new catheter should be
inserted at a different site.
- Foley and drainage catheters should be replaced

59. - Hydrocortisone (50 mg IV every 6 h) should be given; if clinical
improvement occurs over 24–48 h, most physicians would continue
hydrocortisone therapy for 5–7 days before slowly tapering and
discontinuing it

60. Empirical antifungal therapy should be strongly considered if the septic
patient is
• already receiving broad spectrum antibiotics or
• parenteral nutrition,
• has been neutropenic for ≥5 days,
• has had a long-term central venous catheter in place, or
• has been hospitalized in an ICU for a prolonged period.

61. Neurogenic shock
- Interruption of sympathetic vasomotor input after
• a high cervical spinal cord injury,
• inadvertent cephalad migration of spinal anesthesia, or
• devastating head injury may result in neurogenic shock
- In addition to arteriolar dilation, venodilation causes pooling in the
venous system, which decreases venous return and cardiac output

62. - Excessive volumes of fluid may be required to restore normal
hemodynamics if given alone.
- Once hemorrhage has been ruled out, norepinephrine or a pure α-
adrenergic agent (phenylephrine) may be necessary to augment
vascular resistance and maintain an adequate MAP

63. Management Of Obstructive Shock
- Aimed at managing the underlying cause which is usually
surgical

66. References
• Harison’s Principle of Internal Medicine 19th edition
• UptoDate 21.6
• Medscape 2020
• Sepsis Surviving Campaign 2018 guideline
• Management of Hypovolemic shock (www.eMedicine.com)

67. Thank You!