Severe Abdominal Pain Case Study: Sepsis, SIRS, and Organ Failure

This case study presents a 42-year-old male patient experiencing severe abdominal pain, diagnosed with peritonitis caused by a ruptured appendix. The assignment delves into the pathophysiology of sepsis and systemic inflammatory response syndrome (SIRS), discussing how these conditions disrupt the cardiovascular, respiratory, and renal systems. It analyzes the mechanisms of inflammation, cytokine release, and the progression from peritonitis to sepsis. The student examines the treatment administered, including intravenous broad-spectrum antibiotics and surgical intervention (laparotomy), in relation to halting the development of SIRS and preventing organ failure. The case study explores the impact of SIRS on various organ systems, detailing the dilation of blood vessels, tissue damage, and organ dysfunction. It also highlights the importance of clinical decision-making and the role of early intervention in managing the patient's condition, referencing relevant medical literature and research findings.

Running head: SEVERE ABDOMINAL PAIN CASE STUDY
Severe Abdominal Pain Case Study
Name of Student
Name of University
Author Note

1SEVERE ABDOMINAL PAIN CASE STUDY
The rapid treatment by medical staff, helped the progression of peritonitis into full blown
sepsis( a form of systemic inflammatory response syndrome-SIRS). With reference to
pathophysiology, discuss the mechanisms of sepsis and SIRS and how it can disrupt the
normal functioning of the cardiovascular (e.g., significant reduction in blood pressure
despite increased heart rate), respiratory and renal systems. In your answer discuss the
reasons why the described treatment was administered in relation to attempting to halt the
development of SIRS.
In the given case study, a subsequent peritonitis was the reason of acute abdominal pain
and on-time intravenous broad-spectrum antibiotics administration helped to prevent the
development of sepsis (Mishra et al. 2014). Peritonitis is the inflammation of the inner wall of
abdomen called peritoneum that supports and protects the abdominal organs caused by bacteria
or fungal infection. Peritonitis is a serious condition that requires prompt antibiotics
administration for treating the infection. The symptoms depend on the underlying cause of the
infection. Fever, chills, nausea, abdominal rigidity and pain are the common symptoms that were
manifested in the 42-year-old male. Peritonitis from the extraperitoneal source inflammation
occurs from hematogens dissemination (Wu et al. 2013). It is caused by a single microorganism
Escherichia coli, accounting for 70% of the infection that includes fluid resuscitation and
antibiotics administration.
Innate immune system is the non specific immunity that occurs since birth and protects
the body from pathogens and recruits macrophages, mast cells and leucocytes that kill the
pathogen non-specifically. These cells cause inflammation in the affected area and release
cytokines that in turn start the humoral immunity and complement system to kill the antigen

2SEVERE ABDOMINAL PAIN CASE STUDY
(Mishra 2014). The innate immune system’s respond to peritonitis condition is orchestration and
beneficial for the expression of inflammatory cytokines (Mossie 2013). Cytokines are the
membrane-bound small proteins of ±8 - 80 kDa that plays a central role in the negative and
positive immune responses and integration of these reactions to physiological systems such as
hematopoietic and complement systems (Hecker et al. 2014). They act by binding to the specific
receptors on the cell membrane on target cells triggering a cascade of reactions like induction,
inhibition or enhancement of cytokine-regulated genes in the target cell nucleus that modulates
immunological activity of the cell. During peritonitis, mesothelial cells, reticuloendothelial cells,
TNF-α and PMϕ. IL-1β secrete cytokines where they are the primary mediators and leading
players of the inflammatory response (Mishra et al. 2014). There is uncontrolled activation of
systemic inflammatory cascade by these cytokines that has worse outcomes for the patient.
Therefore, peritonitis triggers a peritoneal and acute systemic innate immune response where
there is release of pro and anti-inflammatory responses.
Cytokines play a crucial role in the mediation of immune response of body and
development of systemic inflammatory response syndrome (SIRS). SIRS is the condition when
peritonitis is left untreated that leads to severe complications like fever, chills, tachycardia and
high respiratory rate (Wada et al. 2013). When it is untreated, it extend beyond the peritoneum
that may cause bloodstream infection and sepsis which is a life-threatening and rapidly
progressing condition that can lead to organ failure and shock (Khanna et al. 2013). The
intraperitoneal or abscess cytokine response has serious implications for the host. Research
suggests that bacterial peritonitis is associated with compartmentalized immense intraperitoneal
cytokine response. SIRS is an intensive and nonspecific reaction that is elicited by bacterial
infection in peritonitis. There is complex homeostatic disturbance as there is potential destructive

3SEVERE ABDOMINAL PAIN CASE STUDY
action on the body affecting due to the defensive reaction. The cytokinetic inflammation caused
by the peritonitis gives rise to self-defence mechanism in response to traumatic, infectious or
chemical stimuli (Zarbock Gomez and Kellum 2014). Due to rupturing of the appendix in the
patient, there is ischemia and necrosis and as a result, the bacteria begins to leak out through the
walls, forms pus and suppuration. This appendiceal rupture causes peritonitis that leads to sepsis
and SIRS. The complication of appendicitis led to the SIRS in the patient and release of necrotic
factors like TNF-α.
The patient suffered a ruptured appendix, followed by peritonitis which triggered the
SIRS reaction (Mishra et al. 2014). Immediately after the SIRS is triggered, cytokines are
released to stimulate the inflammatory response of the immune system so that repair mechanisms
can be implemented by the reticulo-endothelial system to recruit mononuclear phagocytes
(Mossie 2013). Cytokines then enter into the circulatory system to enhance the wound repair
mechanism and stimulate growth factors, macrophages as well as platelets. Acute phase response
is commenced with the release of endogenous antagonist and pro-inflammatory mediators to
achieve homeostasis (Khanna et al. 2013). When the body fails to restore homeostasis systemic
allergic reaction is started and influences the cytokines and other associated inflammatory
response cells which starts to destroy the local tissues. The inflammation stimulating mediators
to invade the tissue themselves or recruit other mediators to activate a coagulation cascade,
complement pathway, prostaglandins and leukotrines. The humoral immunity response begins
which reaches the circulatory system, ultimating leading to organ failure, like heart, lungs and
kidney.
The mechanism that leads to the multi-organ failure is described in the following:-

4SEVERE ABDOMINAL PAIN CASE STUDY
 Dilation of the blood vessels due to abnormal distribution of blood throughout the
body.
 The local tissue damage receives influx of inflammatory mediators as well as
other fluids that displace the interstitial cavity between organ and vascular
permeability leading to swelling (Giles et al. 2012).
 Production of reactive oxygen species and proteases by neutrophiles damages
tissues.
 Endothelial tissue damage caused by thrombin production facilitating blood
coagulation.
Dysfunction in the Respiratory System is commonly affected when a patient undergoes
SIRS with the clinical symptoms that including; tachypnoea, hypoxia, chest pain, hypotension
and respiratory acidosis. Prolonged progression of SIRS can lead to acute injury in lungs (ALI)
and acute respiratory distress syndrome (ARDS) (Wada et al. 2013). The respiratory rate
becomes very low which leads to losing the balance between carbon-dioxide (CO2) and oxygen
(O2). This makes causes the respiratory cavity becomes acidic as the bicarbonate level increases.
The pulmonary capillaries become inflammed as a result of which the alveoli sacs become filled
with interstitial fluid due to action of phagocytes and other immunogenic cells. Cytokines invade
the lung tissues and destroy the tissues that cause necrosis of alveolar tissues as well the
basement membrane
The Circulatory System is also vastly affected due to the progression of SIRS.
The cardiac muscles are affected by the pro-inflammation type cytokines along with other
substances that induce acetylcholine production (Vincent et al. 2013). Acetylcholine in turn
activates the pathway that produces nitric oxide from arginine in the vascular endothelium which

5SEVERE ABDOMINAL PAIN CASE STUDY
in turn relaxes the muscles in the circulatory system (Giles et al. 2012). Nitric oxide is a known
vasodilator that makes blood vessels dilated and the pressure of blood in the cardiac cavity is
lowered. This causes the respiratory rate to rise and induce hypoxia which makes the patient feel
breathless (Giles et al. 2012). The condition was severe in case of the patient is suffers from
sinus tachycardia, so this heart was exposed more erratic beats after the commencement of this
syndrome. This phenomenon is termed as hypotension. Cytokines have been known to facilitate
myocardial depression which is correlated with nitric oxide (NO). Excitation in the tissue causes
the NO to move out of the endothelial cells where it activates and binds to guanylyl cyclise
(cGMP), triggering the relaxation of sooth cardiac muscles.
The affect on kidney is also severe in case of SIRS, where the failure in this organ will
disrupts the blood control and excretion in the body affecting the water and ionic homeostasis of
the body. The glomerulus in the kidneys control the urination and water balance in the body,
which is auto-regulated depending on the osmotic pressure in the afferent and efferent arterioles
in the kidney (Cao Harris and Wang 2015). The pro-inflammatory cytokines induce vasodilation
in the arteries that disrupts the whole body’s homeostasis which regulates the acid-base volume,
ionic and electrolyte balance as well as blood pressure. The patient was suffering from
abdominal rigidity due to swelling of the renal system (Hecker et al. 2014) SIRS also induce
macro and micro- circulation in the kidney affecting the protection of vascular tissues, erratic
blood flow and decrease in circulatory density in kidney capillaries. This also affects the
hemodynamic balance maintained by the kidneys which s disrupted by stiffened red blood cells,
white blood cells and platelets that causes swelling in kidney by occluding the capillaries.
Fibrin, thrombins and other coagulation factors also cause blood agglutination and block renal
function (Zarbock Gomez and Kellum 2014).

6SEVERE ABDOMINAL PAIN CASE STUDY
Generally in cases where the patient needs emergency critical care a proper support
system is administered with clinical decision making. The process involves acknowledging the
patient data and analysing the medical data in this case the patient data was clearly indicating
peritonitis symptoms related to pain, tachypnea. The patient came in with severe pain and
stiffness in his abdominal cavity which radiated to his lower right side, which suggested
rupturing of appendix that lead to peritonitis. The clinical decision making support also
recognizes with early warning symptoms that facilitates the rapid response of the staff members
to achieve quick intervention. This is evident when the staff members immediately recognized
the problem which suggests good clinical analytical skills in the staff members. The hospital
staff were quick to analyse the patient’s symptoms, and performed a laparotomy to remove the
appendix and lavaged the peritoneum cavity. Following the surgical procedure the patient was
administered with antibiotics to halt the progression of SIRS. A clinical decision support system
(CDS) offers a systematic application of health-related knowledge and analysis of available data.

7SEVERE ABDOMINAL PAIN CASE STUDY
References:
Cao, Q., Harris, D.C. and Wang, Y., 2015. Macrophages in kidney injury, inflammation, and
fibrosis. Physiology, 30(3), pp.183-194.
Giles, T.D., Sander, G.E., Nossaman, B.D. and Kadowitz, P.J., 2012. Impaired vasodilation in
the pathogenesis of hypertension: focus on nitric oxide, endothelial‐derived hyperpolarizing
factors, and prostaglandins. The Journal of Clinical Hypertension, 14(4), pp.198-205.
Hecker, A., Uhle, F., Schwandner, T., Padberg, W. and Weigand, M.A., 2014. Diagnostics,
therapy and outcome prediction in abdominal sepsis: current standards and future
perspectives. Langenbeck's archives of surgery, 399(1), pp.11-22.
Khanna, A.K., Meher, S., Prakash, S., Tiwary, S.K., Singh, U., Srivastava, A. and Dixit, V.K.,
2013. Comparison of Ranson, Glasgow, MOSS, SIRS, BISAP, APACHE-II, CTSI scores, IL-6,
CRP, and procalcitonin in predicting severity, organ failure, pancreatic necrosis, and mortality in
acute pancreatitis. Hpb Surgery, 2013.
Mishra, S.P., Tiwary, S.K., Mishra, M. and Gupta, S.K., 2014. An introduction of tertiary
peritonitis. Journal of emergencies, trauma, and shock, 7(2), p.121.
Mossie, A., 2013. Pathophysiology of sepsis. World journal of medicine and medical
science, 1(8), pp.159-168.
Vincent, J.L., Opal, S.M., Marshall, J.C. and Tracey, K.J., 2013. Sepsis definitions: time for
change. Lancet (London, England), 381(9868), p.774.

8SEVERE ABDOMINAL PAIN CASE STUDY
Wada, T., Jesmin, S., Gando, S., Yanagida, Y., Mizugaki, A., Sultana, S.N., Zaedi, S. and
Yokota, H., 2013. The role of angiogenic factors and their soluble receptors in acute lung injury
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Wu, H.H., Li, I.J., Weng, C.H., Lee, C.C., Chen, Y.C., Chang, M.Y., Fang, J.T., Hung, C.C.,
Yang, C.W. and Tian, Y.C., 2013. Prophylactic antibiotics for endoscopy-associated peritonitis
in peritoneal dialysis patients. PloS one, 8(8), p.e71532.
Zarbock, A., Gomez, H. and Kellum, J.A., 2014. Sepsis-induced AKI revisited: pathophysiology,
prevention and future therapies. Current opinion in critical care, 20(6), p.588.