Gastroenteritis Assessment - Free Essay Sample

Introduction

Max is a 3-year old presented into the Emergency Department (ED) by his mother at 1600hrs with an 11-hour history of frequent vomiting. Max has been diagnosed with moderate dehydration caused by viral gastroenteritis. There was no history of diarrhea or urination. The child had just been camping with his family, and none of them has related symptoms. For effective healthcare management, this paper attempts to review Max’s circulatory assessment and the underlying pathophysiology of his condition.

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The medical history of Max would be focused on dehydration and severity, including the quantity, duration, and frequency of vomiting, which are critical factors in examining the status. Oral intake, weight loss, and urine output will also be significant considerations. Viruses are anticipated to be a risk factor for acute gastroenteritis if the vomiting is prominent, the incubation period is more than 14 hours, and if the entire condition is over in at most three days. Eating history, travel history (including camping) are critical epidemiological factors. The child has received all immunizations till the current hospitalization episode.

Physical examination of the severity of the condition revealed an alert though irritable and ill-appearing infant having a normal temperature of 37.00C. Max’s respiratory rate was 35 breaths per minute and is relatively hypoxic spo2 (99%) in room air. His pulse rate was 140 beats per minute and blood pressure of 100/65mmHg. Max’s urine output has also diminished.

Upon examining the standard vital signs on Max, I will then undertake a circulatory assessment on him for further examination on the condition.

Physical Assessment

Besides administering measurable observations, including pulse rate and blood pressure, physical observations with a clinical eye are extremely valuable in the diagnosis process of a patient.

Initial impression and behavior – I will examine if Max is active and playful or irritable and weary. Children cannot address how they feel appropriately, so by examining his physical and emotional state, I can accurately reflect the severity of their condition. An alert though irritable and fatigued impression among children, is a sign of dehydration and prompts an immediate intervention (Hartman et al. 2019, p. 159).

Visual assessment – Keen attention to the areas I will be looking at will be very important during this assessment. With adequate room light, I will examine the mucous membranes (including eye wetness) and skin tenting on hands, mouth wetness, capillary refill, and skin color. Dehydrated children will show a dry mouth, tented skin, sunken and dry eyeballs, pale and dry skin, and delayed capillary refill, which are signs of hydration distress (Bányai et al. 2018, p. 175).

Palpation – I will use my hands to palpate Max’s abdomen to sense any presence of tenderness. I will also palpate to examine the condition of his skin to assess his skin temperature and skin turgor. Max is feverish, so his skin is warm, and his abdomen has severe pain and tenderness, suggesting an abdominal emergency (Diskin & Dronen 2017, n.p.).

Measurable Observations

Blood pressure (BP) – Max is hypotensive with a BP of 100/65mmHg, which means that his body is distressed for the delayed capillary refill and skin dryness. Max may pass out soon due to the declining flow of blood if urgent interventions are not taken and increase his blood pressure (Lin & Cagir 2018). Blood pressure is a critical indication of his condition; thus, it must be monitored closely.

Pulse Rate (PR) – Max’s PR is tachycardia (140Bpm). It has elevated due to severe hydration, decreased blood flow, and fluid circulation. Tachycardia is an indication of severe hydration (De et al. 2017, n.p.).

Pathophysiology of Gastroenteritis

Viral gastroenteritis spreads among people by the oral-fecal transmission of water and food that is contaminated. Some viruses, such as norovirus and rotavirus, can be transmitted through the airborne channel (Florez et al. 2020, p. 4). These viruses induce diarrhea by various mechanisms, encompassing adherence, cytotoxin production, enterotoxin production, and mucosal invasion. These mechanisms lead to decreased fluid absorption and increased fluid secretion (Dennehy 2019, p. 157). In turn, there is increased luminal fluid produced that cannot be sufficiently reabsorbed, causing dehydration and loss of nutrients and electrolytes. Gastroenteritis can be classified as osmotic, which occurs because of excessive osmotic load brought into the intestinal lumen, through decreased absorption or excessive intake; inflammatory, which occurs after the inflammation of the intestine’s mucosal lining; secretory, which occurs due to excessive secretory activity; and motile, which is caused by disorders of intestinal mobility (Ikram).

Small intestines act as the main absorptive site of the gastrointestinal tract. Additional fluid is then absorbed by the colon, changing a moderately liquid fecal stream in the cecum into a well-developed solid stool in the rectosigmoid. Small intestine disorders lead to excessive diarrheal fluid amounts with a concurrently high deprivation of nutrients and electrolytes (Hartman et al. 2019, p. 160). Microorganisms may generate toxins that contribute to infection. Enterotoxins, produced by some bacteria – enterotoxigenic vibrio cholera, Escherichia coli - act straight on secretory mechanisms and generate a typical, plentiful watery diarrhea. But it does not cause mucosal invasion.

Small intestines are mainly affected, and an increase in the levels of the adenosine monophosphate (AMP) is the typical pathogenic mechanism. The production of cytotoxin by other bacteria such as Shigella dysenteriae, enterohemorrhagic E coli causes the destruction of the mucosal cell, resulting in bloody stools with inflammatory cells (Bányai et al. 2018, p. 175). In turn, it leads to diminished absorptive ability. Enterocyte invasion enables microbes, including Campylobacter and Shigella bacteria and enteroinvasive E coli result in inflammatory and destruction diarrhea (Diskin & Dronen 2017, n.p.). Equally, Yersinia and Salmonella species also undermine the bloodstream in the lamina propia and can result in enteric fevers, including typhoid. Diarrhea condition occurs when the virulence microbial overwhelms the normal defenses of the host.

Typically, over 100,000 E coli are needed to cause disease; only 10 Entomoeba can suffice to do the same. Some bacteria generate proteins that help their adherence to binding on the walls of the intestine, hence replacing the normal flora and controlling the intestinal lumen (Bányai et al. 2018, p. 177). Besides the pathogen toxins ingestion, other intrinsic factors can cause infection; the change of the normal flora of the bowel can generate a biologic void fulfilled by pathogens (Hartman et al. 2019, p. 162). But this majorly occurs after antibiotic administration; however, infants are also at risk before the colonization with the normal flora of the bowel.

Conclusion

The stomach’s regular PH and colon is an effective defense. But the defense is weakened in achlorhydric states, caused by gastric surgery, antacids, diminished colonic flora anaerobic, and histamine-2 blockers) (Diskin & Dronen 2017, n.p.). Hypomotility conditions can lead to colonization by pathogens, specifically in the proximal small bowel, where mobility is the main way for bacteria removal. Hypomotility can be caused by antiperistaltic agents and is inherent in conditions like scleroderma or diabetes mellitus. The immunocompromised individual is more vulnerable to infection, apparent from the wide diarrheal pathogens spectrum in patients with acquired immunodeficiency syndrome (AIDS) (Bányai et al. 2018, p. 179). The specific causal of vomiting in acute gastroenteritis is not well recognized, but with the release of serotonin as a postulated as a risk factor, inducing visceral afferent input to the chemoreceptor stimulate zone in the lower brainstem (Diskin & Dronen 2017, n.p.). Pre-generated neurotoxins, formed by Bacillus cereus and staphylococcus when ingested, can lead to severe vomiting.

References

Bányai, K., Estes, M.K., Martella, V. and Parashar, U.D., 2018. Viral gastroenteritis. The Lancet, 392(10142), pp.175-186.
https://doi.org/10.1016/S0140-6736(18)31128-0

De, R., Liu, L., Qian, Y., Zhu, R., Deng, J., Wang, F., Sun, Y., Dong, H., Jia, L. and Zhao, L., 2017. Risk of acute gastroenteritis associated with human bocavirus infection in children: A systematic review and meta-analysis. PloS one, 12(9), p.e0184833.
https://doi.org/10.1371/journal.pone.0184833

Dennehy, P.H., 2019. Infectious Gastroenteritis. In Introduction to Clinical Infectious Diseases (pp. 157-168). Springer, Cham.
https://doi.org/10.1007/978-3-319-91080-2_15

Diskin, A., & Dronen, C.D. (2017). Emergent Treatment of Gastroenteritis. MedScape. https://emedicine.medscape.com/article/775277-overview#a4

Florez, I.D., Niño-Serna, L.F. and Beltrán-Arroyave, C.P., 2020. Acute infectious diarrhea and gastroenteritis in children. Current Infectious Disease Reports, 22(2), p.4.
https://doi.org/10.1007/s11908-020-0713-6

Hartman, S., Brown, E., Loomis, E. and Russell, H.A., 2019. Gastroenteritis in children. American family physician, 99(3), pp.159-165.
https://www.aafp.org/afp/2019/0201/p159.html?cmpid=em_AFP_20190201

Ikram, R. (n.d.) Assessment and management of infectious gastroenteritis. Bpac New Zealand. https://bpac.org.nz/BPJ/2009/December/docs/bpj25_gastro_pages10-19.pdf

Lin, B., & Cagir, B. (2018). Viral Gastroenteritis. Medscape.
https://emedicine.medscape.com/article/176515-overview#a5.