and Edgar D. Guzman-Arrieta3
(1)
Department of Surgery Advocate Illinois Masonic Medical Center, University of Illinois Metropolitan Group Hospitals Residency in General Surgery, Chicago, IL, USA
(2)
University of Illinois at Chicago, Chicago, IL, USA
(3)
Vascular Specialists – Hattiesburg Clinic, Hattiesburg, MS, USA
Keywords
Abdominal painVisceral painSomatic painTendernessRebound tenderness1.
All of the following are correct except
(a)
Visceral pain is commonly felt along midline structures.
(b)
Somatic pain has radicular radiation.
(c)
Visceral pain is always the result of organ injury.
(d)
Somatic pain is often lateralized.
(e)
Visceral pain commonly has an insidious onset.
Comments
The clinical presentation of abdominal pain is the result of the complex interaction of pathologic processes stimulating somatic and visceral pain receptors which provide sensory input that the central nervous system interprets, generating autonomic and cognitive responses.
In general, visceral pain is described as ill-defined both in onset and location, dull and nonspecific, often accompanied by autonomic deregulation. Visceral pain is not generated by all viscera such as the liver, kidney, and lung, although their investing layers (Glisson’s capsule, Gerota’s fascia and pleura) are indeed a source of somatic pain. The perception of visceral pain is not directly linked to injury; for example, cutting of the intestine is painless. Visceral pain is often perceived in the midline, perhaps reflecting the original location of the primitive gut. However, it is often associated with radiation which may be lateralized, but retains a fairly ill-defined nature [1].
In contrast, somatic pain is much better defined in its location and time of onset and tends to lateralize. It is not necessarily accompanied by a visceral response, and it is generally linked to injury. Radiation of visceral pain follows a radicular pattern [2] (Fig. 7.1).
Fig. 7.1
Abdominal pain: embryological and anatomical basis
As noted in Fig. 7.1, there is a different perceived location of pain originating from the foregut, midgut, and hindgut, corresponding to the supraumbilical, periumbilical, and infraumbilical areas, which in turn parallels the embryologic location of the vascular supply to either segment and the origin and distribution of visceral pain fibers. Another important clinical feature is that colicky pain originating from obstruction of hollow viscera corresponding to either level has different intervals between spastic episodes, reflecting the baseline peristaltic function of each segment [3] (Fig. 7.2).
Fig. 7.2
Visceral pain is mediated through parasympathetic and sympathetic systems. Parasympathetic nerves travel through the vagus nerve to the foregut and midgut while sacral 2, 3, and 4 nerves innervate the hindgut. Sympathetic nerves travel with celiac, superior mesenteric, and inferior mesenteric vessels to their respective embryological fore-, mid-, and hindguts
In approaching the manifestations of digestive pathology, and the consequences of the surgical interventions to address it, it is useful to liken the GI tract to an internal combustion engine, where the foregut prepares and delivers the fuel, the midgut acts as the engine carrying out the bulk of the work of digestion and absorption, and the hindgut processes the exhaust products (Fig. 7.3).
Fig. 7.3
The endodermal derived foregut extends from the esophagus to the ampulla of Vater and, in the big picture of the GI tract, is largely responsible for storing and mixing the ingested food with the saliva, gastric secretions, bile, and pancreatic enzymes. The midgut, on the other hand, is the main digestive engine responsible for digestion and absorption. The midgut extends from the ampulla of Vater and extends to the right two-thirds of the transverse colon including all of the jejunum and the ileum. The hindgut behaves like the muffler of the engine extending from the lateral one-third of the transverse colon to the rectum. Its main function is to store and evacuate the products of digestive “combustion”
Answer
c
2.
All of the following are correct except:
(a)
The origin and mechanisms of visceral pain are not fully understood.
(b)
Ischemia plays an important role in the transition of visceral to somatic pain.
(c)
The end result of sustained increased intramural pressure is necrosis of the bowel wall.
(d)
Afferent autonomic pain fibers are nonmyelinated.
(e)
There are well-defined visceral pain receptors.
Comments
It is often the case that there is an orderly progression of visceral to somatic pain in the natural history of the majority of inflammatory and obstructive abdominal pathologies.
The exact processes and pathways that originate and mediate visceral pain are not fully elucidated, nor are the distribution of specific visceral pain receptors. In that context, we offer the following hypothesis, centered around the role of perineural lymphatics in the nourishment of nonmyelinated visceral afferent fibers [4–6].
In this model, the onset of hollow viscus visceral pain is brought about by increases in intraluminal pressure that in turn generate elevations in mural pressure that exceed the pressure of the perineural lymphatics, thus interrupting the supply of nutrients to the nerve, generating a distress signal interpreted as pain. As the elevated pressure subsides, pain resolves, until the next cycle (Fig. 7.4).
Fig. 7.4
Receptors of visceral pain
As repeated cycles of increased pressure continue, there is progressive disruption of the normal bowel wall architecture, first with lymphedema, ultimately with an organized inflammatory response, that further enhances pain perception by the delivery of inflammatory mediators that heighten pain perception (Fig. 7.5).
Fig. 7.5
Part I: When increased intraluminal pressure exceeds the low-pressure lymphatic system, we hypothesize that perineural lymphatics are compressed, and that this lack of perineural perfusion to visceral sympathetics manifests as vague, poorly localized visceral pain. The pain will be localized at the embyological origin of the nerve supply along the midline. Clinically, this process results in lymphedema of the wall of the affected viscera producing “woody” edema
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