Plate 2.1
Sensory supply of abdominal viscera and body wall.
The figure can be read from left to right in order to ‘map’ a given source of visceral pain to its conscious appreciation on the body wall, or vice versa, as in the usual context of attempting to diagnose the underlying cause of abdominal pain.
Splanchnic nerves (to abdominal viscera) are shown on left of figure; somatic nerves (to body wall) on right. Spinal cord segments contributing to each nerve (or set of nerves) are shown centrally. In the case of the thoracic (greater, lesser and least), lumbar and sacral splanchnic nerves, the course of the nerve fibres through the sympathetic chain has been omitted for clarity – it is more important to note their levels of origin from the spinal cord.
FG foregut, MG midgut, HG hindgut, CA coeliac axis, SMA superior mesenteric artery, IMA inferior mesenteric artery, IH iliohypogastric nerve, II ilioinguinal nerve
Sensory Nerve Supply
Sensation from the abdominal wall (skin externally, parietal peritoneum internally) is conveyed by the lower 6 intercostal nerves (spinal cord segments T7-12) and the iliohypogastric and ilioinguinal nerves (L1).
Sensation from the abdominal organs (covered in visceral peritoneum) is conveyed by sympathetic supply from the 3 thoracic splanchnic nerves – greater (T5-9), lesser (T10-11) and least (T12) – and the lumbar and sacral splanchnic nerves (cord segments, L1-2). Sensory fibres from the foregut and its derivatives travel back alongside branches of the coeliac trunk to the greater splanchnic nerves (T5-9). Those from the midgut (and gonads) travel along branches of the SMA to the lesser splanchnic nerves (T10-11), and those from the hindgut (along with the urinary tract and uterus) along branches of the IMA (or via a retroperitoneal course) to the least, lumbar and sacral splanchnic nerves (T12-L2).
Additionally, sensation from the pelvic organs (rectum and bladder) is also conveyed by the parasympathetic supply in the pelvic splanchnic nerves to spinal cord segments S2,3,4.
The spinal cord therefore receives 2 sources of sensory input, somatic (body wall) and visceral (organs), which both relay in segments T7-L2. It is this ‘sharing’ of the spinal cord segments which accounts for the phenomenon of referred pain. For example, visceral pain from a midgut structure (e.g. the appendix), conveyed by the lesser splanchnic nerve (T10-11), is referred to the T10-11 dermatome of the abdominal wall by the corresponding intercostal nerves, and is experienced as pain around the umbilicus. Similarly, foregut pain is experienced in the T7-9 dermatomes (epigastrium) and hindgut pain in the T12-L2 dermatomes (hypogastrium). Additionally, pain from pelvic organs can be referred to the S2,3,4 dermatomes and is experienced as pain in the perineum and back of the leg (and easily misinterpreted as sciatica).
Clinical Correlation
The significance of this anatomical principle is further appreciated when assessing the acute abdomen. It is important to realize that although there are many possible diagnoses in the acute abdomen, there are essentially only 2 presentations – obstruction (of a hollow organ) and inflammation (peritonitis, either local or general).
Obstruction
of a hollow organ (intestinal, biliary, renal and uterine tracts) presents as colic – (spasmodic) visceral pain referred to the corresponding dermatomes of the relevant splanchnic nerves.
Inflammation
may be localized to an organ and its visceral peritoneum (a local ‘-itis’ – appendicitis, cholecystitis, etc) or generalized throughout the abdomen, involving both visceral and parietal peritoneum (a general peritonitis – e.g. secondary to a perforated ulcer or tumour). If the inflammation is localized to an organ, (constant) visceral pain will be experienced in the dermatome to which it refers. However, once the inflamed organ makes contact with the overlying parietal peritoneum, (constant) somatic pain will be experienced in the precise location of the overlying intercostal nerve fibres – manifesting as peritonism on examination.
This principle explains the shifting pain of appendicitis – early umbilical colic (visceral) secondary to obstruction of the lumen by a faecolith, shifting to late right iliac fossa pain (somatic) secondary to inflammation of the overlying abdominal wall.
If these underlying principles are applied in a logical manner to the analysis of abdominal pain, the initially overwhelming number of possibilities in the acute abdomen will be reduced to a relatively short list of differential diagnoses, each with a clear anatomical basis.
Assessment of the Limbs
When considering history and examination with regard to the limbs, it is essential to recall the basic tissue types and their organization in the region under review. A logical view is to first consider the internal bony skeleton, with focus on the joint, and then the overlying arrangement of soft tissue, with focus on the muscles and neurovasculature. Attributing a likely pathological process to each structure will then provide a comprehensive list of differential diagnoses.
The Joint
The major joints in the limbs are synovial joints, as distinguished from fibrous and cartilaginous joints. They feature a joint cavity, articular cartilage and a joint capsule, and are usually reinforced by ligaments.
The shape of the articulating surfaces of the two bones comprising the joint, the bony congruency, defines movement and influences stability of the joint. Seven types of synovial joint exist – plane, pivot, hinge , saddle , ellipsoid , condyloid and ball and socket – each allowing a different range of movement. Joints specialized for a high degree of movement are more likely to dislocate. However, bony congruency does not necessarily afford stability, which is more attributable to ligaments and, especially, muscles.
Articular cartilage consists of hyaline cartilage (as distinguished from fibrocartilage and elastic cartilage) on the articular surfaces of synovial joints. It provides resistance to wear and a smooth gliding surface. Repetitive friction over time causes degenerative joint disease – osteoarthritis – particularly in weight-bearing areas, which is an irreversible process due to the avascularity of hyaline cartilage. Some joints also contain discs of fibrocartilage, such as the labrum of the acetabulum and the glenoid, or the menisci of the knee, which increase joint congruency, but can also undergo degeneration and may tear.
The joint capsule is the fibrous casing surrounding the joint surfaces of the articulating bones. It is lined by synovium, the vascular membrane that produces the synovial fluid of the joint cavity, which may become inflamed in inflammatory joint disease .
In certain areas the fibrous capsule may be thickened to form intrinsic ligaments to provide reinforcement. Tearing of the ligament fibres (a “sprain”) occurs when the joint is pulled beyond its normal range of movement. Where intrinsic ligaments do not exist, the capsule may be weaker or deficient, predisposing to the direction of joint dislocation. Extrinsic ligaments also reinforce the joint, yet are discrete from the capsule. A complete tear may produce joint space widening on radiograph; however if their fibres are stronger than the attached bone, they may avulse a bony fragment.
Muscle fibres, or their tendinous attachments to bones, may also similarly tear (a “strain”) or cause bony avulsion. Attrition from pathological bony osteophytes or fractures may cause tendon ruptures. Bursae are synovial lined sacs that exist to cushion muscles and tendons from bony prominences, however they may become inflamed (bursitis) in combination with tendon microtrauma, or discretely infected.
Articular arteries often form significant anastomoses around joints to maintain perfusion with the joint in different positions. However it is important to appreciate that fractures can disrupt perfusion and lead to avascular necrosis.
Hilton’s Law
states that the nerves supplying the muscles that move the joint also supply sensation to that joint and the skin overlying the joint. Joint capsules and ligaments are richly innervated and will readily transmit pain.
The Muscles and Neurovasculature
Body wall musculature develops segmentally in the embryo, with migrating primitive musculature taking its nerve supply with it. The limbs develop from limb buds on the body wall and similarly as the limb muscles undergo migration and rearrangement they maintain their embryonic nerve supply (Plate 2.2).
Plate 2.2
Development of limb musculature.
Transverse section of schematic embryological development of the limbs.
The right side of the diagram shows development of the standard body wall at a thoracic/abdominal segmental level, and the left shows a segmental level of limb development. Note the correlation in neuromuscular origin.
The limb buds are ventral structures developing from the lateral branch of the VPR. This lateral branch divides into a posterior branch for innervation within the extensor compartment of the limb, and an anterior branch (fused with the anterior terminal branch of the VPR) for innervation within the flexor compartment.
BC body cavity, DA dorsal aorta, DPR dorsal primary ramus, DR dorsal root, DRG dorsal root ganglion, GT gut tube, SC spinal cord, SG sympathetic ganglion, VPR ventral primary ramus, VR ventral root
Muscles migrate into flexor and extensor compartments. Their nerves arise from plexuses of ventral (anterior) primary rami derived from cervical and lumbar enlargements of the spinal cord, namely the brachial plexus to the upper limb and the lumbosacral plexus to the lower limb. Anterior divisions of these plexuses supply the flexor compartment and posterior divisions supply the extensor compartment.
The muscles and deep neurovascular structures supplying them are bound by an investing, deep fascia, and divided into compartments by intermuscular septa or interosseus membranes. The fascial compartments allow the muscles to slide freely in contraction, but can cause a compartment syndrome when a muscle pathologically swells, requiring surgical fasciotomy of the compartment. Any anatomical compartment carrying neurovascular structures may cause neuropathic or ischaemic symptoms if the compartment space is reduced or traumatized, for example with inflammatory swellings or fractures (e.g. carpal tunnel syndrome, supracondylar fractures).
Knowledge of myotomes and dermatomes is essential for understanding the effects of spinal nerve lesions on muscular behaviour and sensory skin changes in the limbs. A myotome is an amount of skeletal muscle innervated by a single segment of spinal cord. As a general rule, joint movement is governed by a spinal centre, usually four segments long, where the upper two segments innervate one action, and the lower two innervate the opposite action. Furthermore, the next more distal joint along the limb will be governed by a spinal centre that is (all together) one segment lower in the cord (see Table 2.1).
Table 2.1
Myotomes of the limbs
Upper limba | Lower limb | ||
|---|---|---|---|
Shoulder flex/abd/lat rotation
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