Question: Report each shock including aetiology, brief pathophysiology, and two
treatment modalities. How each shock state differs from each other?
*Septic shock
*Neurogenic shock
*Spinal shock


Septic Shock
Septic shock develops due to systematic response to infection or multiple infection causes
(Dellinger et al. 2013). It is important to note that an individual may have sepsis but that does not
necessarily mean that he/she has septic shock. Some of the infections that can trigger septic
shock when they are severe enough include pneumonia, appendicitis, meningitis, pancreatitis as
well as diverticulitis. These infections cause a constellation of symptoms which present as
disruptions in respiratory rate, heart rate, erythrocyte count, and respiratory rate (Angus & Van
Der Poll, 2013). The infections can worsen leading to end-organ dysfunction to the point where
blood pressure cannot be maintained anymore with intravenous infusion alone; this causes septic
King et al. (2014) report that the pathophysiology of septic shock is not well understood.
However, it has been established that the development of septic shock is linked to an immune as

well as a coagulation response to an infection. Both anti-inflammatory and pro-inflammatory
immune responses contribute to the development of septic shock.
Usually, most septic shock cases are as a result of infection by gram-positive bacteria and
production of endotoxins by gram-negative bacteria (Seymour & Rosengart, 2015). However,
fungal infections have also been cited to be another primary cause of septic shock. The
microorganisms produce toxins which trigger the immune response. The gram-positive bacteria,
which have lipopolysaccharides in their membrane, produce endotoxins.
In response to inflammation, the immune system triggers a compensatory mechanism by
producing anti-inflammatory chemicals, which include interleukin-1 and interleukin ten
antagonists, and cortisol. These chemical substances are generated so that they can suppress the
immune system hence exposing the patients to the risk of secondary infection.
The treatment modality in patients with septic shock is the use of broad-spectrum
antibiotics such as amoxicillin, levofloxacin, or chloramphenicol should be administered within
the first hour after diagnosis of septic shock. Antimicrobial therapy should be done promptly
since the risk of death from septic shock increases by about 10 percent for every hour delayed in
administering the antibiotics (Garnacho-Montero et al. 2014). Due to this risk, the culture,
identification, and testing of antibiotics sensitivity to determine the specific strains of responsible
microorganisms is not done. As a result, combined antimicrobial therapy is preferred since it
covers a broad range of likely causative organisms. The other modality entails infusion of fluids
to the patients because septic shock lowers blood pressure leading to poor tissue perfusion. Fluid
infusion is done so that it can increase the volume of circulating blood (Mouncey et al. 2015).
Lactated Ringer’s solution, as well as crystalloids such as normal saline, are often used as the

initial fluid of choice. Hydroxyethyl starch solution can also be used although studies have not
reported whether it has superior advantages over the crystalloids. Caironi et al. (2014) note that
albumin can also be co-administered with fluids in instances when large amounts of fluids are
infused since it helps in maintaining osmotic pressure in the body.
Neurogenic shock
This form of shock occurs due to the disturbance of the Sympathetic Nervous System
(SNS) leading to loss of the vagal tone. Only the parasympathetic system remains. The shock
arises due to the damage to the vital organs in the central nervous system, that is, the brain,
thoracic or cervical spinal cord (Choi et al. 2015). Trauma hinders sympathetic stimulation of
blood vessels leading to vasodilation, which is followed by a sudden decrease in blood pressure
due to low peripheral vascular resistance.
A neurogenic shock is a distributive form of shock which causes hypotension,
bradycardia due to the disruption of the autonomic pathways within the central nervous system
(Wood et al. 2014). Hypotension occurs due to the reduction of systematic vascular resistance
leading to pooling of blood at the extremities. Conversely, bradycardia presents due to the
unopposed vagal tone. Studies have reported that the bradycardia is exacerbated by hypoxia and
endobronchial suction (Taylor, Wrenn & O’donnell, 2016). It is important to note that neurogenic
shock can cause multiple organ failures followed by death if it is not detected early and treated

Gaieski et al. (2016) point out that in neurogenic shock, treatment aims at stabilizing the
patient and preventing irreversible damage to tissues. Normally, individuals suffering from
neurogenic shock have hypotension which is treated using the intravenous fluid infusion to boost
the blood volume. Vasopressors can also be used to increase the peripheral vascular resistance-
hence increasing hypertension (Lamontagne et al. 2016). Some of the drugs that are administered
to manage hypotension include ephedrine, pseudoephedrine, or epinephrine. The other treatment
modality involves administration of inotropic agents such as dopamine, which aid in increasing
the heart’s pumping force since the patients have bradycardia that inhibits transportation of
oxygenated blood to the extremities.
Spinal Shock
Spinal shock occurs when trauma occurs in the spinal cord. Although spinal shock begins
after a short while after trauma, it may take several hours before its effects are fully observed.
When the shock occurs, transmission of signals by the nervous system fails. Usually, the spinal
shock lasts for about 4 to 6 weeks after the injury. There are cases in which the shock can last for
several months. Lack of signal transmission due to spinal shock hinders the movement and
sensation of an individual as well as how well the systems of the body function (Figley et al.
Spinal shock has been described using mechanisms of injury that last for several hours.
The mechanism of injury that triggers spinal shock is often traumatic. When trauma occurs, the
spinal cord reflex arcs just above the injured level are depressed severely. The pathophysiology
of spinal shock can be due to either primary or secondary injury. The primary injury involves

damage to the neural tissue as a result of direct trauma while secondary injury occurs due to
trauma to adjacent tissue. This can be due to decreased tissue perfusion, peroxidation of lipids, or
apoptosis of cells (Sezer, Akkuş & Uğurlu, 2015). The efferent spinal cord reflex arcs which are
located below the level of trauma are irrevocably changed and serves as sites for basing
rehabilitation efforts.
The first treatment modality entails the use of physical and occupational therapy to aid
the patient to regain his/her functioning. This form of therapy acts as a training regimen that
helps the body to recover from its injuries. The physical therapy also encourages the
development of new neurons in some cases (Kabu et al. 2015). Surgery can also be done on the
patients to get rid of bone fragments or any items that could be lodged in the spinal cord.
Neurogenic shock differs from spinal shock because spinal shock lasts between one to
two days; hence it is temporary (Krishna et al. 2014). The loss of motor and sensory tone are also
temporary. Conversely, neurogenic shock lasts for many days leading to the decrease in muscle
tone due to lack of muscle usage. Unlike the other two forms of shock, that is, septic and spinal
shock, the neurogenic shock is the most difficult to manage because it causes irreversible tissue
damage. The major similarity in these forms of shock is their clinical manifestation because the
patients present with bradycardia and hypotension. Therefore, these symptoms cannot be relied
upon for diagnosis. A detailed patient history is required for a primary diagnosis to be




Angus, D. C., & Van Der Poll, T. (2013). Severe sepsis and septic shock. New England Journal
of Medicine, 369(9), 840-851.
Caironi, P., Tognoni, G., Masson, S., Fumagalli, R., Pesenti, A., Romero, M., … & Iapichino, G.
(2014). Albumin replacement in patients with severe sepsis or septic shock. New England
Journal of Medicine, 370(15), 1412-1421.
Choi, Y. M., Hong, S. H., Lee, C. H., Kang, J. H., & Oh, J. S. (2015). Extracorporeal shock wave
therapy for painful chronic neurogenic heterotopic ossification after traumatic brain
injury: a case report. Annals of rehabilitation medicine, 39(2), 318-322.
Dellinger, R. P., Levy, M. M., Rhodes, A., Annane, D., Gerlach, H., Opal, S. M., … & Osborn, T.
M. (2013). Surviving Sepsis Campaign: international guidelines for management of
severe sepsis and septic shock, 2012. Intensive care medicine, 39(2), 165-228.
Figley, S. A., Khosravi, R., Legasto, J. M., Tseng, Y. F., & Fehlings, M. G. (2014).
Characterization of vascular disruption and blood–spinal cord barrier permeability
following traumatic spinal cord injury. Journal of neurotrauma, 31(6), 541-552.
Gaieski, D. F., Parsons, P. E., Hockberger, R. S., & Finlay, G. (2016). Evaluation of and initial
approach to the adult patient with undifferentiated hypotension and shock. UpToDate,
Waltham, MA. Accessed on February 25th.
Garnacho-Montero, J., Gutiérrez-Pizarraya, A., Escoresca-Ortega, A., Corcia-Palomo, Y.,
Fernández-Delgado, E., Herrera-Melero, I., … & Márquez-Vácaro, J. A. (2014). De-
escalation of empirical therapy is associated with lower mortality in patients with severe
sepsis and septic shock. Intensive care medicine, 40(1), 32-40.

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