intermittent fever, malaise, aches & pain, wt loss
alcohol induced pain
obstructive symptoms due to enlarged lymph nodes
Horner’s syndrome compression on the sympathetic ganglion
Reed-Sternberg giant cells are present in Hodgkin’s lymphoma
thorough clinical examination
laboratory CP, ESR, Urinalysis
imaging CXR, USG abdomen
Bone marrow aspiration
Lymph node biopsy
stage IA, IIA Radiotherapy….90% survival
stage IIIA, IIIB Chemoradiation
oncovin( vincristine )
extensive extra-nodal d/s poor prognosis
Metastatic Lymph Nodes
from primary sites head & neck
history & clinical examination to find out the primary lesions
Metastatic Lymph Nodes 2
surgery for primary lesion is required & node > 3 cm en bloc dissection
--radiotherapy advanced tumours
Blood Supply Superior and inferior thyroid arteries
Venous drainage Superior, middle and inferior thyroid veins
Overview of Method
General Inspection Around the bed, patient
Hands Acropachy, sweaty palms
Face Peaches and cream complexion
Eyes Eye disease
Neck Thyroid, trachea, and lymph nodes
Legs Pretibial myxoedema
Thin / fat
Nervous / agitated
Under-clothed and sweaty
Overdressed but cold
Hoarse ( RLN ) / fatiguable voice ( ELN )
Inspect from the front
Tremor / Restless / Agitation
Hair and Eyebrows
Stand in front of pt
Is This a Thyroid ?
Ask patient to stick tongue out while palpating:
Ask patient to swallow water:
Should NOT move Should move
Inspection of Hands
Pulse (AF / Tachy)
periosteal new bone
Pulse rate, rhythm
Examine from in front
from the side
Upper lid pulled back to expose sclera above iris
On looking up or down, lid doesn’t follow eyeball
Inspect from front - lid retraction
Inspect from side / above ....
Eyes - Graves ’ Disease
Due to retro-orbital inflammation and lymphocyte infiltration.
Sclera visible above and below eye
Weakness of ocular muscles due to oedema & cellular infiltration of these muscles.
Superior & Lateral rectus and inferior oblique muscles are affected mostly.
Paralysis of these muscles prevents the patient looking upwards & outwards.
Palpate from behind
Ask about pain!
Use bimanual palpation
Note character of swelling (one lump / multiple lumps / diffuse enlargement)
Stand behind pt
Thumbs on occiput
Flex neck slightly
Moves on swallowing?
Neck / Chest
Percuss for a retrosternal goitre
Auscultate for a thyroid bruit
Summary Risk Factors Hypothyroidism Hyperthyroidism Family or personal hx of thyroid disease Family or personal hx of thyroid disease Goiter or hx of goiter Goiter or hx of goiter Prior or current thyroid use Prior or current thyroid use Hx of other autoimmune disease Hx of other autoimmune disease Recent iodine exposure
Clinical Findings Hypothyroidism Hyperthyroidism Fatigue Fatigue Weight gain Weight loss without change in appetite Cold intolerance Heat intolerance Depression or memory impairment Depression or nervousness, irritablility, anxiety or agitation Menstural irregularities (menorrhagia), infertility Menstural irregularities (oligomenorrhea) Weakness, muscle cramps, joint pains Weakness, tremor Palpitations Exertional dyspena Constipation Hyperdefecation Hoarseness Anterior neck pain Hypersomnolence Insomnia
Physical Exam: Thyroid----Related Findings Hypothyroidism Hyperthyroidism Xerosis (dry skin) Moist palms (increased perspiration) Thickening of skin, especially pre-tibial Preorbital puffiness Bulging eyes (lid retraction or proptosis ), unblinking stare Eye irritation, periorbital edema, diploplia, change in visual acuity ** Delayed relaxation phase, deep tendon reflex Hyperreflexia Dry Coarse hair or alopecia Bradycardia Tachycardia, atrial fibrillation Non-pitting edema
WOUNDS AP U Kyaw Naing SUII
A wound can be caused by almost any injurious agent and can involve almost any tissue or structure.( due to trauma)
A wound is a breach in continuity of epithelium due to trauma .
An ulcer is a breach in continuity of epithelium.
Classification of wound
Inflicted by sharp instrument
Contain no devitalized tissue
Can be closed primarily with exception of P’ healing . Eg. Surgical wound, cut from glass and knife.
Repair is possible.
Result from crushing, tearing, avulsion vascular injury or burn
Contained devitalised tissue
Must not be closed primarily
T – wound excision
Healthy Healing Surgical Wound
Wounds may be classified as
Contaminated – eg. Bowel perforation
Dirty – eg. fecal contamination
Types of wound
Wound healing is the summation of a number of processed which follow injury including
Phase 1 : inflmmation
Phase 2 : cell proliferation & matrix formation
Phase 3 : matrix remodelling
Phase 1 : Inflammation
PMN polymorpho-nuclear leucocytes
3 – 4 days
Phase 2 : Cell proliferation & matrix formation
New capillary & matrix systhesis
Collagen, proteoglycan & glycoprotein
Phase 3 : Matrix remodelling
Reorientation of collagen fibrils
Process Cell Type Mediator
Wounding injured cell phospholipase of
Coagulation platelets IL-1, PDGF, TGF-B
Inflammation L FGF
Angiogenesis Gr TGF-B
Proteoglycan Syn Fibroblast
Epithelialisation Epithelial cell EGF
( Biological Process in wound repair )
Healing by Primary Intention
Haemostasis – clotting cascade
Pro: of inflammation
Cell proliferation and migration
Epidermal cell migration - covering
Arrival of neutrophil and macrophage
Demolition and removal of exudate and debris
Restoration of tensile strength
Secretion of chemoattractant
Expansion of fibroblast
Stimulation of fibroblast to secrete extracellular connective tissue
Healing by Second Intention
A large wound of tissue loss
Movement of wound margin
Contraction – myofibroblast fibronectin
Endocrine, paracrine, autocrine pathway
PDGF, EGF, TGF@ and B
Stages of Bone Healing
Woven bone formation
Factors affecting wound healing
General factors Local factors
1. Age 1. Blood supply
2. Vitamin – C, Zinx 2. Infection
3. Diabetic 3. Haematoma
4. Jaundice & Uraemia 4. Faulty technique
5. Cytotoxic drug 5. Tension
6. Malignancy 6. Steriod
7. Infection – pus 7. Oxygen
8. Immunocompromised Pt
Did this person jump or was he blown out of the building?
Somebody knew what was coming...
Do you think just any lawn would hold up like this after a plane crashed on it?
Not a Scratch! Perfect Lawn!
Lower Limb - Fasciotomy
A survivable airway problem
Exsanguinating Pelvic Trauma
Infection , Haemorrhage
Clostridium tetani is the bacterium that causes tetanus, and it is mainly found in the soil.
In developed countries, most cases occur in older adults.
In developing countries, about half of the cases of tetanus are found in neonates.
There are four main types of tetanus
Symptoms of tetanus are cause by disinhibition of the nervous system.
The source of a tetanus infection is a wound, where Clostridium tetani enters the body.
The Discovery of Tetanus
Hippocrates (right) was said to describe tetanus as far back as the 5 th century B.C.
Nicolaier first produced tetanus in animal specimens.
Kitasato isolated the organism from a human victim and neutralized the toxin.
How Tetanus Was Discovered
The bacterium Clostridium tetani is abundant in soil and Tetanus was produced by injecting soil specimens in animals.
Less than 100 cases per year in the UK
More prevalent in developing countries
Following deep or penetrating wound in relatively avascular areas
Gram-positive rod with terminal spores
(drum stick appearance).
A strict anaerobe
Produce powerful exotoxin.
Exotoxin causes muscle spasms and rigidity
Spores of Clostridium tetani live in feces, soil, dust an on instrument.
The spores enter through tiniest breach in skin and mucous membrane
They may then germinate and produce exotoxin.
This travel up peripheral nerves and interferes with inhibitory synapse.
Reduces the release of inhibitory neurotransmitters
Excess activity of motor neurones produces muscle spasm
Clostridium tetani usually enters the body through a wound.
The spores germinate, and two toxins are produced:
The toxin starts out as a polypeptide, and changes into two chains.
The heavy chain travels to the central nervous system, which activates the light chain.
The light chain releases an inhibitor which causes muscle spasms to occur.
Incubation period ( time of injury to first symptom)- 7-10 days, sometimes up to years.
Period of onset (first symptom to first reflex spasm) - 5-7 days
Prodromal symptoms (fever, malaise, headache)
Trismus (patient can not open his mouth)
Risus sardonicus (a grin-like posture of hypertonic facial muscles)
Opisthotonus (arched body with hyperextended neck)
spasms (at first may be induced by stimulus but later are spontaneous)
Dysphagia and respiratory arrest
autonomic dysfunction (arrythmias, wide fluctuation in BP)
Bad prognostic signs
Short incubation period
Rapid progression from trismus to spasms (<48 hours)
Tetanus in neonates and old age
Begin about 8 days after infection.
“ Lockjaw” or trismus occurs, which is muscle stiffness in the jaw.
Severe muscle spasms occur, bringing many complications:
Fracture of spine or long bones
Flexion of arms and legs
History of injury or presence of wound is used.
History of parental drug use or personal IV drug use strengthens diagnosis.
Differential diagnosis includes:
Painful conditions of the lower jaw is included
Abnormalities in the peripheral nervous system
Appropriate history and physical examination can differentiate most of these.
The treatment involves:
Neutralizing the toxin
Removing the source of the toxin
Supportive care for muscle spasms, respiration, and autonomic instability
Recovered patients must receive a tetanus immunization series, due to the fact that survivors of tetanus have a greater risk of getting it again.
Passive immunization with human immune globulin shortens the course of tetanus and may lesson severity.
Penicillin and metronidazole are the antibiotics commonly used.
The spasms cause by tetanus can be extremely harmful and cause many complications.
Sedatives can be used to control spasms.
Neuromuscular blocking agents are used to relax muscles.
Metronidazole, diazepam, and benzodiazepine and most commonly used to control spasms.
Management General treatment
Hospitalised the patient
Isolate the patient in quiet and comfortable place with dim lighting.
Change the position to prevent pressure sore
Clean wounds, debride as necessary
Use i.v. penicillin or metronidazole for 7 days to destroy the bacteria
Human tetanus immune globulin (HTIG) 500 U i.m. to neutralise free toxin
Antitetanus toxoid to get active ammunity
Analgesic for muscle pain
Fluid therapy for daily requirement
Care and maintenance of airway during cyanotic convulsion
Specific treatment depends on severity of disease
Stage 1. Mild case (Tonic rigidity alone)
Initial sedation, relaxation by drugs
promazine up to 200 mg. and a barbiturate or diazepan.
Feeding orally +/- IV fluid
Stage 2. A seriously ill patient
Dysphagia and reflex spasm.
Feeding by nasogastric tube or total parenteral nutrition
Tracheostomy should be considered if the patients has any difficulty in breathing.
Stage 3. Dangerously ill patients
A major cyanotic convulsion
curarisation to maintain relaxation.
Intermittent positive-pressure ventilation should be provided.
Feeding - total parenteral nutrition, IV fluid
Intensive nursing care
2 hourly position change to prevent bedsore
Indwelling urinary catheter change
Care of tracheostomy, parenteral feeding and feeding line
If recovery takes place, the patient can be weaned from ventilator.
Prevention Prevention of high risk group
Pregnant mother ( ATT - first dose at 28 weeks, second dose-6weeks later, third dose-6 weeks after delivery)
Infant - ATT 3 doses during infancy and booster dose at 5 years.
Farmers, labourers - ATT - 3 doses( 6 weeks after first and 6 months after second) . Booster dose for ever 5 years or at the time of injury.
Prevention at the time of injury
Thorough wound debridement
Penicillin to kill the Cl. tetani
Patient with adequate immunisation
booster dose of ATT
Patient with inadequate or no immunisation
small risk wound - ATT
High risk wound - ATT plus human antitetanus globulin
followed by second and third dose of ATT at 6 weeks and 6 months interval
The death rate is high in children and the elderly.
The worldwide mortality rate is 50%, and it is 30% in the United States.
Drug users have a high rate of death because of complications due to the drug.
Untreated tetanus is usually fatal within a few weeks.
The four types of tetanus all have different mortality rates.
Generalized tetanus has a 50% mortality rate.
Local tetanus has a 1% mortality rate.
Neonatal tetanus has a 70% mortality rate.
Cepahic tetanus has a 15-30% mortality rate.
The amount of tetanus bound to the nerves affects prognosis, and the more toxin, the poorer the prognosis.
Surgical removal of damaged tissue and medical treatment improve prognosis.