Osteochondritis is sometimes classified as-

1. Crushing type or Osteochondrosis
2. Osteochondritis dissecans
3. Tractions Osteochondritis or traction apophysistis

Common Osteochnodrites –

1. Perthes’ disease – Head of femur is affected
2. Panner’s disease- Capitulum affected
3. Kienbock’s disease- Lunate bone affected
4. Osgood-shlatter’s disease- Tibial tuberosity Osteochondritis
5. Sever’s disease- Calcaneal tuberosity Osteochondritis
6. Kohler’s disease- Navicular bone affected
7. Freiberg’s Disease- Metatarsal head affected
8. Scheurmann’s disease- Ring epiphyses of vertebra affected
9. Calve’s disease- Centralbody of nucleus of vertebral body affected.

Perthes’ Disease:-

Aka. Coxa Plana, Pseudocoxalgia

This is the Osteochondritis of the epiphysis of the femoral head. In the disease, the femoral head becomes partially or completely avascular and deformed as well.

Cause- not exactly known. ? recurrent ischemia of head of femur in susceptible age group. Usually precipitated by Synovitis

Age Group Susceptible- 5- 10 years                          Gender- Boys> Girls

Stages:

1. Stage of synovitis

2.Stage of Trabecular necrosis

3.Stage of healing

Presentation-

• Pain in the hip region, pain may radiate to knees.
• Hipstiffness and limping may be present
• On examination- not much findings, sometimes there is shortening of the affected limb, and the limb may be externally rotated and abducted.

X-Ray- Collapse and sclerosis od the epiphysis of the femoral head. Joint space increased- hip joint.

Bone scan- decreased uptake by femoral head.

Treatment-

Principle- preventing the Head from deforming in the softening phase, while keeping it in acetabulaum while revascularization takes place (Head Containment)

Methods- Plaster, special Braces, Splints, Operation- containment- osteotomy.

Further Reading:

AAOS

Patients Reading: patientcouk

Anatomy of Carpal Tunnel:

Carpal tunnel is a narrow passageway in the wrist formed by:

Posterior side: 8 carpal bones

Anterior side: Transverse carpal ligament

Contents:

9 Flexor tendons

Median Nerve

Median Nerve Distribution in Hand:

Origin: From lateral and medial cords of brachial plexus

Motor innervation:

Lumbricals: 1st and 2nd

Muscles of thenar eminence: Opponens pollicis, Abductor Pollicis Brevis and Flexor Pollicis Brevis)

Mnemonic: LOAF (Lumbricals, Opponens pollicis, Abductor Pollicis Brevis and Flexor Pollicis Brevis)

Sensory innervation:

Skin of the palmar side of the thumb, the index and middle finger, half the ring finger, and the nail bed of these fingers (3 and 1/2 digits)

Lateral part of the palm by palmar cutaneous nerve (unaffected in Carpal tunnel syndrome)

Carpal Tunnel Syndrome

It is a syndrome characterized by the compression of the median nerve as it passes beneath the flexor retinaculum in carpal tunnel.

Causes:

Any space occupying lesion (SOL) of carpal tunnel can cause carpal tunnel syndrome -

Inflammatory causes:

• Rheumatoid arthritis
• Wrist osteoarthritis

Post-traumatic causes:

• Colle’s fracture

Endocrine causes:

• Myxoedema
• Acromegaly

Idiopathic

Mnemonic: MEDIAN TRAP

• Myxoedema
• Edema premenstrually
• Diabetes
• Idiopathic
• Acromegaly
• Neoplasm
• Trauma
• Rheumatoid arthritis
• Amyloidosis
• Pregnancy

Clinical features:

It usually occurs in females between the age of 40 and 70. They complain of tingling, numbness or discomfort in the lateral 3 and 1/2 fingers i.e. distribution of median nerve. They also complain of intermittent attacks of pain in the distribution of the median nerve on one or both sides. The attacks frequently occur at night. The reason symptoms are worse at night may be related to the flexed-wrist sleeping position and/or fluid accumulating around the wrist and hand while lying flat. Pain may be referred proximally to the forearm and arm.

Motor changes: Ape-like thumb deformity, loss of opposition of thumb, index and middle fingers lag behind when making the fist

Sensory changes: Loss of sensations on lateral 3 and 1/2 digits including the nail beds and distal phalanges on dorsum of hand

Vasomotor changes: The skin areas with sensory loss is warmer due to arteriolar dilation; it is also drier due to absence of sweating due to loss of sympathetic supply

Tropic changes: Long-standing cases of paralysis lead to dry and scaly skin. The nails crack easily with atrophy of the pulp of fingers.

Tests

To approximate where along the wrist the median nerve runs, gently flex and radially (laterally) deviate your wrist. Two tendons will become palpable and even visible—palmaris longus (in midline) and flexor carpi radialis

(lateral to it). However, 15% of people do not have a palmaris longus muscle. The median nerve runs deep between these tendons.

Phalen’s Test:

Bend the patient’s wrists downwards as shown in the figure

This position should be held for about 1 minute.

Positive test : numbness or tingling along the median nerve distribution

Tinel’s Test:

With the palm up, tap over the carpal tunnel area of the wrist 5 or 6 times

Positive test : tingling or paresthesia in the median nerve distribution

Durkan Test:

Press thumb over carpal tunnel and hold pressure for 30 seconds.

Positive test: Onset of pain or paresthesia in the median nerve distribution

Electromyogram (EMG)

Nerve conuction studies are done for diagnosis these days

Treatment

1. Immobilizing braces/Splints
2. Analgesics like NSAIDs
3. Local injection of steroids
4. Surgery: Dividing the flexor retinaculum

Carpal Tunnel Syndrome as Occupational Disease

Causes:

1. repetitive hand motions
2. awkward hand positions
3. strong gripping
4. mechanical stress on the palm
5. vibration

Common occupations:

1. Cashiers
2. Hairdressers
3. Knitters
4. Farmers (milking cow)
5. Office workers (keyboarding)
6. Painter, etc.

May be allergic or hemolytic

1. Hemolytic reactions: can be acute or delayed

Acute Hemolytic reactions:

• It is usely due to ABO incompatibility, there is intravascular hemolysis
• As low as 10 ml of blood can produce hemolytic reactions
• Clinically, patients presents with complains of pain and burning in vein and fever with chills and rigor, nausea and vomiting, flushing, chest and flank pain and dyspnea.
• It is confirmed by hemoglobinuria
• ARF can occur due to blockage of tubules

Management:

• Stop infusion
• Recheck the blood details
• Maintain urine output by mannitol and fruit administration
• Alkalinize urine
• Hemodialysis

Delayed Hemolytic Reactions:

• Are extravascular hemolytic reactions
• Mainly due to Rh system and other system incompatibility eg. Kell Duffy
• These reactions are mild and seen after 21 days
• Diagnosed by Coomb’s test
• Treatment is supportive

2. Allergic reaction:

• These are mainly mild, seen as urticaria and are mainly due to plasma proteins
• Treatment is antihistaminics and steroids
• If anaphylaxis occurs, stop transfusion
• Adrenaline and steroids

B. Febrile Reactions:

Due to infusion of white cell microaggregates
Can be minimized by using microfilter blood sets with pore size 20-40 micrometer
Generally require no treatment

C. Infectious Complications:

• Hepatitis: 90% are due to hepatitis C virus
• HIV/AIDS
• Other viral diseases like CMV, EBV, HTLV-1, HTLV-2, parvovirus
• Bacterial infections like Pseudomonas, Staphylococcus, Syphillis, Brucellosis, Salmonella, Yirsenia and rickettsial disease
• Parasitic infections like malaria, toxoplasmosis, filariasis, trypanosomiasis, Creuz-Jackobs Disease (prion)

D. Fluid Overloading and Pulmonary Edema

E. Metabolic Complications:

• Hyperkalemia
• Hypocalcemia
• Acid-base abnormalities

F. Coagulation abnormailities:

Occurs due to dilution of coagulation factors and platelets
Treatment is fresh blood
Fresh frozen Plasma
Specific blood components therapy
Platelets

G. Hypothermia: Blood should be warmed before use

H. Immunosuppression- graft vs host reaction

I. Tissue hypoxia – due to shift of oxygen dissociation curve to left due to decreased 2,3 DPG

J. Endotoxaemia and Septicaemia

K. ARDS (Acute Respiratory Distress Syndrome) – now known as TRALI (Transfusion Related Acute Lung Injury)

L. Disseminated Intravascular Coagulation (DIC)

DEFINITION:-

Shock is an acute clinical syndrome characterized by poor tissue perfusion with impaired cellular metabolism, which is manifested as different serious pathophysiological abnormalities.

Shocked patient

CLASSIFICATION OF SHOCK

Hypovolaemia

Cardiogenic

Intrinsic

Compressive

Septic

Hyperdynamic

Hypodynamic

Anaphylactic

Traumatic

Neurogenic

Hypoadrenal

CAUSES OF SHOCK

Hypovolaemia shock:- due to reduction in total Blood volume.

Loss of blood:- hemorrhagic shock, RTA, major surgeries.

Loss of plasma:- burn shock, pancreatitis.

Loss of fluid:- diarrhea, vomiting , renal loss of water, DI etc.

Septic shock:-

Due to bacterial infxn and its toxins.

Cardiogenic shock:-

Acute MI, Acute carditis

Acute pulmonary thromboembolism

Toxaemia of any cause

Cardiac compression due to cardiac temponade or trauma.

Neurogenic shock:-

Due to sudden anxious or painful stimuli causing splanchnic vasodilatation

Anaphylactic shock

Type I hypersensitivity rxn

Penicillin, anesthetics, stings, venoms, shellfish

Others:-

Addison’s disease

myxoedema

PATHOPHYSIOLOGY OF SHOCK

• low CO
• vasoconstriction in vital organs(Brain, kidney, heart, liver.)
• Minute volume 1.5 – 2 times increased
• RR :- 2 – 3 times increased
• Decreased blood flow to kidney
• Decreased GFR and urinary output
• Release of ADH and activation of RAS  and increased aldosterone.
• Increased water retention and decreased urine output.

• As CO falls
• hypotension and tachycardia
• Decreased coronary perfusion
• This in conjunction with hypoxia causes Metabolic Acidosis
• Release of specific cardiac depressant
• Further pump failure.

• Due to lack of oxygen in cells
• Anaerobic respiration- lactic acidosis
• Na+ K- pump failure -hyperkalaemia
• Calcium enters the cells- hypocalcaemia
• further intracellular lysosome breakdown and release powerful enzymes causing further damage
• Sick cell syndrome

• Platelets are activated forming small clots in many places
• DIC ( consumption coagulopathy)
• Further Bleeding
• 
  

HYPOVOLAEMIC SHOCK

CONVERT COMPENSATED HYPOVOLAEMIA:-

Presence of reduced circulating blood volume without very obvious associated physical sign.

Often difficult to diagnose.

In conscious ptn CNS features are best guide

CF:- Nausea, drowsiness, hiccups, thirst.

Lab inv:- urine analysis:- increased urinary osmolality and decreased Na+ concn.

OVERT COMPENSATED HYPOVOLAEMIA

Here there is hypovolumia to an extent then reflex mechanism required to maintain perfusion to the vital organs.

O/E:- tachycardai, tachapnoea , wide arterial pulse pressure, systolic BP increased, pale, cool clammy extremities., drowsiness, confusion.

if diagnosis is uncertain:- Gentle head down ,bed tilting

Leg raising or administration of iv bolus fluid.

if diagnosis is true

Increase venous return , decrease HR, narrow pulse pressure , reduce RR, and overall well being improved.

ABG analysis:- hypoxaemia, metabolic acidosis.

DECOMPENSATED HYPOVOLAEMIA:-

Severe degree of hypovolaemia

reflex mechanism insufficient to compensate blood flow to vital organ. So decreased perfusion of vital organs.

C/F:- Mean arterial pressure falls

Tachycardia changes to Bradycardia

Conscious level severely compromised

Coma

Peripheral Pulses impalpable

Decreased CO

V/P- mismatch.

MANAGEMENT

HISTORY:- h/o  blood loss, fluid loss, plasma loss.

C/F:- depends on the type of hypovolaemia.

DIAGNOSIS:- depends on clinical monitoring and investigation.

CLINICAL MONITORING :-

VITALS:-

HR:- rate :- tachycardia then later bradycardia.

rhythm may be thready and irregular

RR:- tachapnoea

BP:-systolic BP increased.

TEMP:- may be normal.

URINARY OUTPUT:- decreased.

INVESTIGATIONS:-

PULSE OXYMETER:- to determine venous oxygen saturation.

ABG analysis:- hypoxemia , metabolic acidosis.

SERUM  ELECTROLYTE:-

hyperkalaemia, hypocalcaemia, metabolic acidosis.

CVP:-

PCWP:-

ECG:- to monitor or detect cardiac arrhythmia.

CHEST X-RAY:- mediastinal trauma or cardiac tamponade.

USG ABDOMEN:- to detect intra abdominal Hge from spleen and liver

TREATMENT

OBJECTIVE:- to treat the cause

to increase CO

to improve tissue perfusion( coronary, cerebral, renal and mesenteric vascular beds)

Hospitalize the patient:-

Airway / Breathing should be secured

O2 inhalation, intubation, artificial ventilation if required.

Intravenous line:- to be opened with wide bore canula as soon as possible.

infuse crystalloid (R/L) or colloid ( albumin, gelatin, haemaccel ,hetastarch

If it is a case of HAEMORRHAGE:-

Take specific measure to control hemorrhage :-

Pressure packing,

Position and rest

Tourniquet

Surgical methods.

immediately send the blood for cross matching and transfusion of Blood as soon as possible.

IONOTROPHIC DRUGS:-

DOPAMINE ( 3 – 10gm/kg/min) .iv-improves renal and splanchnic blood

DOBUTAMINE ( 2 – 8 gm/kg/min) :- Improves CO

CORRECT ACID BASE AND ELECTROLYTE BALANCE

SEPTIC SHOCK

Cause:- due to Gm -ve  and Gm +ve organism, fungi, viruses and protozoa

Gm -ve septicaemia is also known as endotoxic shock.

Commonly seen in strangulated intestine, peritonitis m GI fistula, urinary infxn, pancreatitis, major surgical wounds etc.

Pathophysiology of septic shock

• Toxins , endotoxins from Gm -ve organism( E.coli, klebsiella, pseudomonas and proteus)
• Inflammation, cellular activation( macrophages,neutrophils, monocytes)
• Release of cytokines free radicals
• Chemotaxis of cells. Endothelial injury, altered coagulation cascade-SIRS.
• Reversible hyperdynamic warm stage of septic shock with fever, tachycardia, tachypnoea
• Severe circulatory failure wit MODS ( failure of lungs, kidneys, liver , heart) with DIC
• Hypodynamic, irreversible cold stage of septic shock.

STAGES OF SEPTIC SHOCK

HYPERDYNAMIC ( WARM ) SHOCK:-

Reversible stage

Pyrogenic response is still intact.

C/F:- fever , tachycardia and tachypnoea

warm dry skin

HYPODYNAMIC ( COLD) SHOCK:-

Decompensated shock

Pyrogenic response is lost.

Irreversible stage along with MODS.

Generalized capillary permeability , leakage causes hypovolaemia, decreased CO , tachycardia, vasoconstriction

C/F:- cold clammy skin, drowsy, tachapnoeic

Investigation:-

Culture & sensitivity :- Blood, Pus , Urine.

USG/ CT:-To find out source of infection.

Treatment of septic shock

• Correction of fluid and electrolyte by crystalloids , blood transfusion.
• Start antibiotics of high generation like cephalosporin, aminoglycosides, metronidazole.
• Treat the cause or focus:- drainage of abscess, laparotomy for peritonitis, resection of gangrenous bowel wound excision.
• Critical care, O2, ventilator support, dobutamine /dopamine /NA to maintain BP and urine output.
• Activated protein C :- prevent release and block the effect of inflammatory mediator on cellular function.
• Monitor:- pulse, BP, RR, urinary output, level of consciousness.

CARDIOGENIC SHOCK

Here intravascular volume is Normal or increased.

Cardiac dysfunction limits the cardiac output and leads to:-

Raised lf atrial pressure

Increased pulmonary artery pressure

Pulmonary edema

Raised Rt ventricular overload and failure.

Causes:-

myocarditis, Acute MI, cardiomyopathy, dysarrhythmia

congenital and acquired heart disease ,metabolic derangement,

Drug intoxication and poisons.

Treatment

Bed rest

Propped position

O2 inhalation

Vitals monitoring

Volume expansion( iv fluids)

Drugs:- dopamine or

dobutamine + epinephrine.

After load reducing agent:- nitroprusside , milrinone.

Deteriorating Cardiogenic shock:- Lf ventricular assisted device

Rt ventricular assisted device.

Anaphylactic shock

PATHOPHYSIOLOGY- antigens  combine with IgE of mast cells  and basophils , releasing  histamine and large amount of SRS-A

CAUSES- Injections- penicillin , anaesthetics , stings, venoms

C/F- sudden onset

bronchospasm , laryngeal oedema

Generalised rashes, oedema

respiratory distress , hypotension , feeble pulse

T/T- Oxygen with  foot end elevation

IV fluids

Adrenaline 100g IV, Antihistaminics, steroids,

Ventilator  in  severe cases

Cardiac massage , defibrillation