Page 129 - Textbook of Pathology, 6th Edition

Microscopically, the changes are noticeable if ischaemia infarction in which case the deeper layers of gut (muscu- 113
is prolonged for 12 to 24 hours. Neurons, particularly laris and serosa) are also damaged. In shock due to burns,
Purkinje cells, are more prone to develop the effects of acute stress ulcers of the stomach or duodenum may occur
ischaemia. The cytoplasm of the affected neurons is and are known as Curling’s ulcers.
intensely eosinophilic and the nucleus is small pyknotic. Grossly, the lesions are multifocal and widely distributed
Dead and dying nerve cells are replaced by gliosis.
throughout the bowel. The lesions are superficial ulcers, CHAPTER 5
2. HEART IN SHOCK. Heart is more vulnerable to the reddish purple in colour. The adjoining bowel mucosa is
effects of hypoxia than any other organ. Heart is affected oedematous and haemorrhagic.
in cardiogenic as well as in other forms of shock. There Microscopically, the involved surface of the bowel shows
are 2 types of morphologic changes in heart in all types of dilated and congested vessels and haemorrhagic necrosis
shock: of the mucosa and sometimes submucosa. Secondary
i) Haemorrhages and necrosis. There may be small or large infection may supervene and condition may progress into
ischaemic areas or infarcts, particularly located in the pseudomembranous enterocolitis.
subepicardial and subendocardial region. 7. LIVER IN SHOCK. Grossly, faint nutmeg appearance
ii)Zonal lesions. These are opaque transverse contraction is seen.
bands in the myocytes near the intercalated disc. Microscopically, depending upon the time lapse between
3. SHOCK LUNG. Lungs due to dual blood supply are injury and cell death, ischaemic shrinkage, hydropic
generally not affected by hypovolaemic shock but in septic change, focal necrosis, or fatty change may be seen. Liver
shock the morphologic changes in lungs are quite function may be impaired.
prominent termed ‘shock lung’. 8. OTHER ORGANS. Other organs such as lymph nodes,
spleen and pancreas may also show foci of necrosis in
Grossly, the lungs are heavy and wet. shock. In addition, the patients who survive acute phase
Microscopically, changes of adult respiratory distress of shock succumb to overwhelming infection due to Derangements of Homeostasis and Haemodynamics
syndrome (ARDS) are seen (Chapter 17). Briefly, the altered immune status and host defense mechanism.
changes include congestion, interstitial and alveolar
oedema, interstitial lymphocytic infiltrate, alveolar hyaline
membranes, thickening and fibrosis of alveolar septa, and Clinical Features and Complications
fibrin and platelet thrombi in the pulmonary The classical features of decompensated shock are
microvasculature. characterised by depression of 4 vital processes:
4. SHOCK KIDNEY. One of the important complications Very low blood pressure
of shock is irreversible renal injury, first noted in persons Subnormal temperature
who sustained crush injuries in building collapses in air Feeble and irregular pulse
raids in World War II. The renal ischaemia following Shallow and sighing respiration
systemic hypotension is considered responsible for renal In addition, the patients in shock have pale face, sunken
changes in shock. The end-result is generally anuria and eyes, weakness, cold and clammy skin.
death. Life-threatening complications in shock are due to
hypoxic cell injury resulting in immuno-inflammatory
Grossly, the kidneys are soft and swollen. Sectioned responses and activation of various cascades (clotting,
surface shows blurred architectural markings. complement, kinin). These include the following*:
Microscopically, the tubular lesions are seen at all levels 1. Acute respiratory distress syndrome (ARDS)
of nephron and are referred to as acute tubular necrosis 2. Disseminated intravascular coagulation (DIC)
(ATN) which can occur following other causes besides 3. Acute renal failure (ARF)
shock (Chapter 22). If extensive muscle injury or 4. Multiple organ dysfunction syndrome (MODS)
intravascular haemolysis are also associated, peculiar With progression of the condition, the patient may develop
brown tubular casts are seen. stupor, coma and death.
5. ADRENALS IN SHOCK. The adrenals show stress
response in shock. This includes release of aldosterone in CIRCULATORY DISTURBANCES OF
response to hypoxic kidney, release of glucocorticoids OBSTRUCTIVE NATURE
from adrenal cortex and catecholamines like adrenaline THROMBOSIS
from adrenal medulla. In severe shock, acute adrenal
haemorrhagic necrosis may occur. Definition and Effects
6. HAEMORRHAGIC GASTROENTEROPATHY. The Thrombosis is the process of formation of solid mass in
hypoperfusion of the alimentary tract in conditions such circulation from the constituents of flowing blood; the mass
as shock and cardiac failure may result in mucosal and itself is called a thrombus. In contrast, a blood clot is the mass
mural infarction called haemorrhagic gastroenteropathy of coagulated blood formed in vitro e.g. in a test tube.
(Chapter 20). This type of non-occlusive ischaemic injury
of bowel must be distinguished from full-fledged *Major complications of shock can be remembered from acronym
ADAM: A = ARDS; D = DIC, A = ARF; M = MODS.