Acute Inflammation (Appendicitis and Meningitis)

Question 1

Appendix Information

Answer 1

Extends from inferior tip of the caecum No obvious function Averages 6-7cm in length, 0.7cm in diameter Mesoappendix - portion of the mesentery connecting the ileum to the appendix The histologic structure is similar to colon The lining in younger persons is interspersed with lymphoid follicles.

Question 2

Who does Acute appendicitis primarily affect?

Answer 2

Disease of developed countries Adolescents Young adults Can however, occur at any age

Question 3

Main reason for acute appendicitis?

Answer 3

Luminal obstruction (50 - 80%) fecalith gallstone tumour ball of worms

Question 4

Explain Pathogenesis of Acute Appendicitis

Answer 4

Luminal obstruction in minority of cases (fecalith, lymphoid hyperplasia) Continued secretion of mucous —> Increased pressure Possible mucosal ischaemia Mucosal injury Acute mucosal inflammation Secondary bacterial invasion Spread of inflammation transmurally

Question 5

Three stages of Acute Appendicitis

Answer 5

Early acute appendicitis (mucosal inflammation) Acute suppurative appendicitis (transmural inflammation) Acute gangrenous appendicitis (necrosis through muscularis propria)

Question 6

Morphology of Early Acute appendicitis

Answer 6

Neutrophilic exudate in mucosa Mild vasodilation

Question 7

Morphology of Suppurative appendicitis

Answer 7

Inflammation spreads transmurally Mucosal ulceration and purulent exudate in lumen Fibrinopurulent exudate over inflamed serosa Dilated congested blood vessels +/- microabscess formation in wall

Question 8

Morphology of Acute gangrenous appendicitis

Answer 8

Necrosis extending through the muscularis propria Followed quickly by rupture and acute peritonitis

Question 9

Why does necrosis and ulceration develop?

Answer 9

Large numbers of neutrophils releasing enzymes and oxygen derived free radicals from ganules Also from bacterial toxins

Question 10

Macroscopic features of acute suppurative appendicitis

Answer 10

The serosa will appear erythematous and be covered by a patchy pale fibrionopurulent exudate The appendix is likely to be tense and the walls thickened There may be mucosal ulceration and necrosis or pus (seen as viscous cloudy fluid) in the wall There may be solid faces (feacolith) and pus (seen as viscous cloudy fluid) in the lumen.

Question 11

Clinical features of acute appendicitis

Answer 11

Abdominal pain, tenderness Low grade fever Nausea +/- vomiting Anorexia Neutrophilia Large differential diagnosis including mesenteric lymphadenitis etc.

Question 12

Why is diagnosis of acute appendicitis very hard in the young?

Answer 12

Because the young are unable to tell you where the pain is originating from, therefore you don’t know where to treat.

Question 13

Discuss the pain associated with acute appendicitis

Answer 13

Initially: Vague midabdominal/perimbilical discomfort Continuous +/- cramps Due to stretching and inflammation of the appendix during the early acute inflammatory period (visceral pain) Several hours later: Pain increases Shifts to R iliac fossa Maybe discomfort on walking or coughing Localised tenderness Becomes localised and more severe as the inflammatory process extends to involve the serosal layer of the appendix and the adjacent parietal peritoneum

Question 14

What are the complications of acute appendicitis?

Answer 14

Perforation due to transmural necrosis –> spread of faecal organisms into peritoneal cavity —> generalised peritonitis or localised periappendiceal abscess: More severe pain Higher fever More likely in very young and elderly Early surgical intervention is thus warrented to prevent this

Question 15

What is generalised peritonitis?

Answer 15

Complication of acute apendicitis. Severe abdominal tenderness and rigidity Ileus and abdominal distension (temporary arrest of intestinal peristalsis) High fever Rapid progression to septic shock

Question 16

What is acute suppurative peritonitis?

Answer 16

Complication of acute appendicitis. Acute inflammation with lots of neutrophils and necrotic inflammatory exudate (pus) involving the peritoneal lining. Arises following rupture of a necrotis inflamed appendix > spillage of faecal contents into the peritoneal cavity > infection Necrosis of the appendix wall is caused by enzymes and oxygen derived free radicals released from neutrophils and also bacterial infection

Question 17

What is septic shock?

Answer 17

Complication of acute appendicitis. Septic shock frequently develops as a complication of generalised acute peritonitis due to gram negative bacteria entering and proliferating in the blood stream. Inflammatory response occurs to the gram negative bacteria in the blood leading to their death. Lipopolysaccharides in the bacterial cell walls are released which in large amounts lead to systemic endothelial injury and the release of cytokines causing widespread vasodilation, increased vascular permeability and myocardial injury. These lead to decreased BP and shock.

Question 18

What are the meninges?

Answer 18

Three layers covering the brain Dura mater Arachnoid mater Pia mater

Question 19

How are CNS infections classified?

Answer 19

According to structures affect Nature of the infecting organism e.g. bacterial, viral e.g. meninges - meningitis parenchyma - encephalitis spinal cord - myelitis brain and spinal cord - encephalomyelitis

Question 20

4 routes of infection in the nervous system. What are they?

Answer 20

Haematogenous spread - most common route of entry, normally via the arterial circulation Direct implantation - almost invariably taumatic - very rarely iatrogenic e.g. lumbar puncture, can be associated with congenital malformations Local extension - infection in sinus, tooth or sugical site leads to osteomyelitis - bone erosion and propagation of the infection in the CNS Via the peripheral NS into the CNS e.g. herpes simplex and rabies

Question 21

How can damage to nervous tissue occur?

Answer 21

Direct injury by the infectious agent Indirectly through the action of microbial toxins Destructive effects of the inflammatory response Immune mediated mechanisms

Question 22

Meningitis

Answer 22

Associated with inflammation of the pia mater, the arachnoid membrane and the CSF containing subarachnoid space The inflammation normally spreads rapidly because of the circulation of CSF around the brain and the spinal cord The inflammation associated with meningitis is normally caused by infection, but it may be triggered by non-infective inflammation (e.g. chemical meningitis)

Question 23

What is Bacterial Meningitis?

Answer 23

Also referred to as acute pyogenic meningitis The microorganisms that cause meningitis tend to vary with the age of the patient

Question 24

What bacteria in bacterial meningitis affects neonates?

Answer 24

E.coli and group B streptococci

Question 25

What bacteria in bacterial meningitis affects Infants and children

Answer 25

Used to be H. influenzae Now streptococcus pneumoniae

Question 26

What bacteria in bacterial meningitis affects Adolescents and young adults

Answer 26

Neisseria meningitis

Question 27

What bacteria in bacterial meningitis affects Elderly

Answer 27

Streptococcus pneumoniae Listeria monocytogenes

Question 28

Common signs of Bacterial Meningitis?

Answer 28

Headache Photophobia Irritability Clouding of consciousness Neck stiffness Bulging fontanelle (babies) Nuchal rigidity (pus in SAS in severe cases can cause spasming of the back muscles

Question 29

How to know if you bacterial meningitis?

Answer 29

Spinal tap reveals cloudy or purulent CSF, which is under increased pressure High neutrophil count - as many as 90,000/mm3 Raised protein level and markedly reduced glucose levels Bacteria may be seen on smear, or can be cultured

Question 30

How to treat?

Answer 30

Usually with antimicrobial agent

Question 31

What are some complications of Bacterial meningitis?

Answer 31

Cerebral oedema and raised ICP Extension of infection into brain itself: Focal cerebritis If patient survives long enough there will be organisation of exudate —> adhesions Adhesions may caused: Blockage of CSF flow —> hydrocephalus Compression of cranial nerves —> cranial nerve palsies Involvement of blood vessels —> thrombosis —> infarcts Septic shock

Question 32

What is Meningococcaemia?

Answer 32

Replication of meningococcus releases large amounts of endotoxin This endotoxin from bacterial cell wall interacts with macrophages to release cytokines and free radicals These substances damage vascular endothelium, resulting in platelet deposition and vasculitis This leads to vascular disruption and petechiae Most dire complication of this is water house friderichsen syndrome, which is multi organ shock.

Question 33

Macroscopic features to Bacterial Meningitis

Answer 33

Brain is swollen and leptomeninges are congested Purulent exudate in SAS over cerebral hemispheres and base of brain May see oedematous white matter and compressed ventricles Ventricular enlargement due to obstructive hydrocephalus

Question 34

Microscopic features to Bacterial Meningitis

Answer 34

In severe cases neutrophils fill the entire subarachnoid space In less severe cases/areas PMN are found around leptomeningeal blood vessels

Question 35

What is the other word for Bacterial Meningitis?

Answer 35

Acute Pyogenic Meningitis