Hello fellow AMBOSSians! I’m Dr. Zeb, back with another question walkthrough that requires us
to diagnose and know how to treat a type of shock that is very important for your exams
and clinical work. So click on the link in the top left... yep... here to follow along!
Let’s first check out the lead-in so we know what to do.
“Which of the following is the most appropriate next step in pharmacotherapy?”
Ok, we need to figure out what the patient likely has, so let’s read a sentence or
two before to see if we can already get some important diagnostic clues.
“The results of blood and urine cultures are pending. Fluid
resuscitation and broad-spectrum antibiotic therapy are initiated.
After 2.5 L of 0.9% saline infusion, his blood pressure is 78/54 mm Hg.”
Alright, this information is already quite revealing.
Considering his blood pressure is still very low despite fluid resuscitation,
what should we be thinking?
That’s right: shock.
And in order to determine how to proceed,
we need to know what type. So what are the different types of shock?
Static electricity, outlets, electric eel, lightning… pfff...
Okay, obviously not electric shocks - we're talking about circulatory, and that would be?
Hypovolemic, for example, due to hemorrhage or extreme gastrointestinal fluid loss.
Cardiogenic, like after myocardial infarction or arrhythmias.
We have, of course, obstructive, such as with cardiac tamponade or tension pneumothorax.
And there's also distributive shock and its subtypes, including
anaphylactic, neurogenic, and septic shock.
Now, considering the context of pending cultures and antibiotic therapy, we already have a pretty
good idea of what form we’re dealing with here, of course, and that would be septic shock.
And honestly, if I was taking a timed exam,
I would probably try to answer the question already here to save some time. But I’d like
to go over some of the vignette to highlight a few key features that you should know.
Before I do that, what is a really handy way of predicting if a patient has septic shock?
The qSOFA score, which is considered positive if 2 or more of the following are present:
altered mental status, systolic BP of 100 or less, or a respiratory rate of 200.... haha...
(Beep)
Ah, no - not 200 - 22 or more.
There are also other sepsis screening tools,
including SIRS criteria, which are summarized in this part of the Sepsis AMBOSS article:
Note that there are conflicting data and opinions regarding the use of sepsis screening tools
for diagnosis or predicting mortality rate that goes beyond the scope of this video. Regardless,
they are associated with improved patient care and can help in identifying at-risk patients.
So let’s read from the top and keep an eye out for signs that are consistent with these features.
“A 68-year-old man with bilateral percutaneous nephrostomy tubes is
brought to the emergency department by his wife because of altered mental status…”
Okay, we already have 2 out of the 3 features for qSOFA.
I’d really feel comfortable answering at this point, but let's quickly read
over a few more points so we have context for all of the concepts we’re reviewing.
So “ She adds that, after both nephrostomy tubes were exchanged 4 days ago, the urine
output from the right nephrostomy bag was relatively low, and that he complained of
right flank pain yesterday.” Let’s skip to the vitals: “His temperature is 36.8°C (98.2°F),”
Remember that sepsis can still occur in afebrile and even hypothermic patients,
especially in older or younger individuals,
and is even an indicator of poorer prognosis that requires more aggressive management.
“...pulse is 124/min,” so tachycardia - a SIRS criterium.
“...respirations are 22/min,” so slightly elevated,
fulfilling the third of the qSOFA criteria and also a SIRS criterium.
“...and blood pressure is 76/50 mm Hg when supine.”
Let’s skip to: “The right nephrostomy bag contains a small amount of cloudy urine;
the left nephrostomy bag contains clear urine.”
What are the question writers trying to tell us here?
Yes, of course - the source of the sepsis is a urinary infection of the
right nephrostomy tube secondary to obstruction.
“Hemoglobin concentration is 12 g/dL,
leukocyte count is 22,000/mm3,” - so elevated and also fitting SIRS criteria for sepsis.
“...platelet count is 180,000/mm3, and serum lactic acid concentration is 4.2
mmol/L.” - also elevated, and an important indicator of sepsis that can guide treatment.
Now let's move on... “hemodynamic monitoring shows:
Pulmonary capillary wedge pressure (PCWP) of 4 millimeters of mercury” - so decreased.
Systemic vascular resistance (so SVR) of 455” - so decreased.
Cardiac index of 5.3” - so increased.
Mixed oxygen venous saturation (SvO2) of 81%” - also increased.
Okay, let’s put on our thinking caps and answer the question:
For this patient with septic shock and persistent hypotension despite initial treatment with fluids,
what drug should we administer to raise blood pressure?
Norepinephrine is correct.
Shocking, huh?...
As you’ll remember with septic shock, circulatory bacterial toxins and cytokines cause capillary
leakage and vasodilation, which leads to a decrease in both systemic vascular resistance
(in other words, afterload) and PCWP (so preload). The body tries to compensate by
increasing the heart rate and cardiac output. Peripheral microcirculatory shunting leads to
lower oxygen extraction, resulting in an elevated mixed oxygen venous saturation.
And this is where norepinephrine can help: Its primary mechanism of action is activating alpha-1
receptors, causing vasoconstriction and increasing SVR (so afterload)
to counter the effects of sepsis. Despite the increase to afterload,
cardiac output typically remains stable as beta-1 inotropy increases to compensate.
With an explanation of the correct answer behind us,
let’s check out some of the other options to see what concepts we can learn or reinforce.
Phenylephrine, as an α-adrenergic agonist (predominantly α1), is a vasopressor with
mainly vasoconstrictive properties. It's sometimes used in treatment of neurogenic
shock. While this patient’s hypotension and low PCWP match neurogenic shock,
we’d expect a history of traumatic brain or spinal cord injury, bradycardia with low cardiac output,
and a low SvO2 because of higher oxygen extraction due to slower peripheral blood flow.
Phenylephrine would only be considered as a second-line vasopressor in septic shock.
Dopamine, as an inotropic agent, was previously used for septic shock,
as it was thought to be renoprotective. But it’s no longer recommended as a first-line treatment
for septic and cardiogenic shock because of the higher risk of tachyarrhythmia and death.
It should only be considered as an alternative vasopressor in select cases
(for example, for patients with a low risk of tachyarrhythmia, or with bradycardia).
Dobutamine, an inotrope that causes vasodilation, is indicated for cardiogenic shock. Unlike here,
this type of shock typically results in a high PCWP and normal or low SvO2 due to an increased
oxygen extraction from peripheral tissue hypoxia. There were also no underlying causes
for cardiogenic shock like myocardial infarction or cardiomyopathy. For septic shock, dobutamine
should only be considered for hypoperfusion that persists despite fluids and initial vasopressors.
Corticosteroids such as hydrocortisone cause vasoconstriction by inhibiting inflammatory
mediators like histamine and are used in the treatment of anaphylactic shock. As
a type of distributive shock, it can also manifest with low PCPW,
high cardiac output, low SVR, and elevated SvO2.
However, anaphylactic shock occurs within minutes to hours of exposure to an antigen
and coincides with additional findings like urticaria, dyspnea, and abdominal pain. With
that said, hydrocortisone may be considered in septic shock refractory to the first vasopressor.
As for no additional pharmacotherapy, failure to maintain a mean arterial pressure of 65 or
more after fluid resuscitation is an indication for pharmacotherapy
Now, what other questions could you get for a vignette like this?
They might have asked for the underlying cause as we discussed.
Or the most likely pathogen of this cause of urosepsis, which would be E. coli,
or other Gram-negative bacilli such as Proteus, Enterobacter, Klebsiella,
or Pseudomonas. Also, Staphylococcus saprophyticus
is possible. The mnemonic SEEK PP as you see here in AMBOSS can help you remember these.
So in another question, they could have taken the
table out and asked about a matching set of expected parameters, as we discussed.
They might have asked for any of the diagnostic or management steps right after examination,
such as serum lactate, blood and urine cultures, fluid resuscitation with normal saline, or empiric
antibiotic therapy, all of which you can review in more detail in the Sepsis AMBOSS article.
Make sure you know these concepts, as any of them could appear on your exams for this topic.
To conclude, the key takeaways of this question are:
Identify the different types of shock and when to suspect septic shock based
on clinical findings like hypotension, tachycardia, increased respiratory rate,
altered mental status, and a likely source such as a complicated urinary infection.
Understand their supporting lab and hemodynamic values, like leukocytosis, elevated lactic acid,
low PCWP and SVR, and elevated cardiac output and mixed oxygen venous saturation.
Know how to manage septic shock, including initial fluid resuscitation and empiric antibiotics,
and norepinephrine for persistent hypotension despite initial fluids.
And that’s it for this question! Let me know with a thumbs up and comment if you found it helpful
and feel free to subscribe for future videos by clicking
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I wish you all happy studying! Remember that hard work pays off,
so keep it up and stay positive. You’ve got this.