COMMON FOOT INFECTIONS

COMMON FOOT INFECTIONS

pediagenosis    November 20, 2024    Comment   

COMMON FOOT INFECTIONS

COMMON INFECTIONS OF FOOT

The foot exists in an environment that unfortunately can be conducive to infection. Primarily, the use of shoes constricts the foot and produces a warm, moist environment that encourages bacterial growth. Foot infections can occur in all individuals. But, the diabetic patient is particularly susceptible to foot infection owing to the loss of protective sensation. Even trivial trauma either from a poorly fitting shoe or from bare-foot walking can result in violation of the skin and lead to severe infection. Poor blood supply and diminished immune function further compromise the diabetic patient’s ability to fight foot infection. Common locations for foot infections include the paronychial (nail) area and the deep spaces of the foot.

DIABETIC FOOT ULCERATION

DIABETIC FOOT ULCERATION

pediagenosis    November 20, 2024    Comment   

DIABETIC FOOT ULCERATION

LESIONS OF THE DIABETIC FOOT

Patients with diabetes are susceptible to a host of foot-related problems. One of the most common and troublesome problems is ulceration and subsequent infection of the foot. Ulceration of the foot develops in the diabetic patient primarily as a result of peripheral neuropathy and loss of the normal protective sensation. Whereas the individual with normal protective sensation would immediately sense minor trauma such as the rubbing of a shoe and take immediate steps to correct it, the diabetic individual is not aware of the problem, allowing the pressure to continue unabated. Eventually, even minor repetitive trauma can result in formation of an ulcer. Ulcers occur most commonly on the weight-bearing plantar surface of the foot and over bony prominences. Once ulceration develops, it is also more likely to become infected in the diabetic patient owing to diminished immune function and impaired circulation. Failure to sense the normal signs of infection due to neuropathy can result in progression to osteomyelitis and extensive, limb-threatening infection in the diabetic patient.

AMPUTATIONS IN THE FOOT

AMPUTATIONS IN THE FOOT

pediagenosis    November 20, 2024    Comment   

AMPUTATIONS IN THE FOOT

AMPUTATION OF FOOT

Amputation of all or a portion of the foot represents the most elemental form of foot surgery. Often it is disparaged by the surgeon, perhaps because it can be perceived as a failure of treatment. But when performed properly, amputation is truly a reconstructive procedure that can eradicate infection, correct deformity, decrease pain, and improve function.

TUBEROUS SCLEROSIS

TUBEROUS SCLEROSIS

pediagenosis    November 19, 2024    Comment   

TUBEROUS SCLEROSIS

TUBEROUS SCLEROSIS

Tuberous sclerosis (Bourneville’s syndrome) is a multisystem disease that often manifests with cutaneous findings. It is inherited in an autosomal dominant manner and is directly caused by a defect in one of two genes, TSC1 or TSC2, usually due to a spontaneous mutation. TSC1 has been shown to encode the hamartin protein, whereas TSC2 gene encodes the tuberin protein. The skin, central nervous system (CNS), cardiovascular, respiratory, visual, and musculoskeletal systems are affected. This genodermatosis has an extremely variable phenotype. At one extreme is the severely disabled and mentally delayed individual with severe seizure disorders; at the other end of the spectrum is the individual with mild skin disease and unappreciable CNS disease.

NEUROFIBROMATOSIS

NEUROFIBROMATOSIS

pediagenosis    November 19, 2024    Comment   

NEUROFIBROMATOSIS

CUTANEOUS MANIFESTATIONS OF NEUROFIBROMATOSIS

There are eight distinct clinical forms of neurofibromatosis. The two most studied and clinically important forms are type I and type II. Neurofibromatosis type I (von Recklinghausen disease) and neurofibromatosis type II are autosomal dominant disorders involving the skin, the central nervous system, and various other organ systems. Type II has many overlapping features that are also seen in patients with type I disease. The genetic bases for type I and type II neurofibromatosis have been determined, and the specific gene for each type has been isolated. The skin findings can be instrumental in the diagnosis of neurofibromatosis type I.

Delayed Or Absent Puberty

Delayed Or Absent Puberty

pediagenosis    November 19, 2024    Comment   

Delayed Or Absent Puberty

Delayed puberty is defined as the absence of secondary sexual characteristics at age 13 in girls and 16 in boys (Chapters 11 and 12). It may result from: (i) a nonpathologic constitutional delay accompanying a growth delay; (ii) disorders of the hypothalamus or pituitary gland that result in inadequate gonadotropin secretion (hypogonadotropic hypogonadism); and (iii) disorders of the gonads that prevent adequate sex steroid secretion (hypergonadotropic hypogonadism) (Table 29.1). In girls, secondary sexual characteristics may develop without progression to menarche. This form of pubertal dysfunction and other causes of primary amenorrhoea are discussed in Chapter 30. It is important to diagnose and treat delayed or absent puberty because: (i) serious underlying conditions may be present; (ii) abnormal persistence of a child-like phenotype has profound social implications for the teenager and young adult; (iii) prolonged absence of gonadal steroid exposure leads to osteopenia, a failure of normal bone formation. Osteopenia is associated with an increased risk of fractures in weight-bearing bones such as vertebrae, hips and long bones. Treatment of delayed or absent puberty aims to correct underlying disorders. Hormone replacement with estrogen/progesterone or testosterone is often required if hypogonadism is prolonged or age-appropriate sex steroid secretion patterns cannot be restored.

Neurofibroma

Neurofibroma

pediagenosis    November 19, 2024    Comment   

Neurofibroma

Neurofibromas are uncommon benign skin tumors that can be solitary but are more commonly found in multiples in patients with neurofibromatosis. Neurofibromatosis is one of the more common genodermatoses, afflicting 1 in every 3000 to 4000 individuals. It is caused by a defective tumor suppressor gene.

Venous Drainage of Small and Large Intestines

Venous Drainage of Small and Large Intestines

pediagenosis    November 10, 2024    Comment   

Venous Drainage of Small and Large Intestines

VEINS OF SMALL INTESTINE

The veins that drain blood from the small and large intestines largely parallel the arteries that supply each organ and share the same names. However, because the veins eventually drain to the hepatic portal vein and liver, there are some notable departures from the arterial scheme. The superior mesenteric vein drains the midgut organs and receives blood from the inferior pancreaticoduodenal, jejunal and ileal, ileocolic, and right and middle colic veins. These veins run parallel to the concordantly named arteries as they leave the superior mesenteric artery, although blood is flowing in the opposite direction from blood in the arteries. Because of its position near the superior mesenteric vein and the fact that there is no celiac vein, the right gastroomental vein drains to the right side of the superior mesenteric vein shortly before the latter drains into the hepatic portal vein. The artery of the same name is a branch of the gastroduodenal artery, which branches from the common hepatic artery and celiac trunk.

Blood Supply of Small and Large Intestines

Blood Supply of Small and Large Intestines

pediagenosis    November 10, 2024    Comment   

Blood Supply of Small and Large Intestines

ARTERIES OF SMALL INTESTINE

The blood supply to the small and large intestines is extremely variable and unpredictable. The variations concerning the origin, course, anastomoses, and distribution of the intestinal vessels are so frequent and so significant that conventional textbook descriptions are inadequate and, in many respects, even misleading, a situation much the same as that of the blood supply of the upper abdominal organs. Because of this variability, the surgeon should have an intimate acquaintance with the entire spectrum of the gut’s arterial supply in order to avoid operative errors, such as devascularization of intestinal sections, which might inadvertently induce necrosis leading to rupture and peritonitis. In this overview, we will review the most typical branching patterns of the vessels associated with the small and large intestines. In the sections devoted to each organ, we will consider the complex variations that may be encountered.

ATRIA AND VENTRICLES

ATRIA AND VENTRICLES

pediagenosis    November 07, 2024    Comment   

ATRIA AND VENTRICLES

RIGHT ATRIUM AND RIGHT VENTRICLE 

Right Atrium

The right atrium consists of two parts: (1) a posterior smooth-walled part derived from the embryonic sinus venosus, into which enter the superior and inferior venae cavae, and (2) a thin walled trabeculated part that constitutes the original embryonic right atrium. The two parts of the atrium are separated by a ridge of muscle. This ridge, the crista terminalis (see Plate 1-7), is most prominent superiorly, next to the SVC orifice, then fades out to the right of the IVC ostium. Its position corresponds to that of the sulcus terminalis externally (see Plate 1-6). Often described as a remnant of the embryonic right venous valve. the crista terminalis actually lies just to the right of the valve.