Shoulder dystocia
Is the impaction of the anterior fetal shoulder against the symphysis pubis after delivery of the head.

It is detected early by observing the head tightly pulled back against the perineum, this is called “Turtle sign”.

Management

HELPERR
H: call for help
E: evaluation for episiotomy
L: legs (McRobers maneuver)
- hyperflexion of the hips
-abduction of hips
- flexion of the knees.
P: external pressure on the suprapubic area.
E: enter “rotational maneuver”
R: remove posterior arm (deliver it)
R: roll the mother on her all fours ( hands and knees).

If all above procedures failed :
- Symphysiotomy
- fetal clavicle fracture
- Zavanelli maneuver ( push the head inside the uterus and proceed with emergency caesarean.

اتذكر الدكتورة گالت اذا مات الطفل نگص راسة ونطلع الباقي بالـ caesarean

Diagram of subdural haematoma

Antero-posterior radiogram of the skull. A bilateral chronic subdural haematoma has been evacuated through two burr holes. Air has entered through these and revealed the bilateral depression on the convexity of cerebral hemispheres produced by the two haematomas.

It is also called acute inflammatory demyelinating polyradiculoneuropathy (AIDP). It is a neurological disorder in which the body's immune system attacks the peripheral nervous system, the part of the nervous system outside the brain and spinal cord. The onset of GBS can be quite sudden and unexpected and requires immediate hospitalization. It can develop over a few days, or it may take up to several weeks with the greatest weakness occurring within the first couple of
weeks after symptoms appear.

It often develops after a respiratory or gastrointestinal viral infection, surgery, injury, or a reaction to an immunization.

In GBS the immune system starts to destroy the myelin sheath that surrounds the axons of many nerve cells, and, sometimes, the axons themselves. When this occurs, the nerves can’t send signals efficiently, the muscles lose their ability to respond to the commands of the brain, and the brain receives fewer sensory signals from the rest of the body. The result is an inability to feel heat, pain, and other sensations.

Note/ facial nerve is the most commonly involved nerve.

At first symptoms begin as weakness or tingling sensations in the legs which sometimes spreads to the arms and upper body. A neurological exam usually reveals a loss of all deep tendon reflexes “Areflexia”

Unique signs and symptoms to GBS:

- Symptoms on both sides of the body (symmetrical)

- Symptoms appear quickly, days or weeks instead of months Loss of reflexes (rapid progressive illness)

- High protein level in cerebral spinal fluid -by lumbar puncture- ( CSF protein levels correlate with the number of demyelinating electrophysiologic criteria abnormalities, starting from > 45 mg/dl for those who meet one criteria of demyelination).

The goal of treatment is to prevent breathing problems and relieve symptoms, in addition to immune system suppressing by Plasmapheresis (a procedure used to remove the plasma and replace it with other fluids. Antibodies are also removed with the plasma), and IVIG (intravenous immunoglobulin), other supportive therapies like hormonal and physical to increase muscle flexibility and strength.

هذا أعراضه كلش nonspecific
لغرض التبسيط، فهي أما تكون cardiovascular (wet beriberi)
أو تكون neurological (dry beriberi) أو مزيج من الإثنين

• while Guillain-Barré syndrome (GBS) is an important cause of acute flaccid paralysis, thiamine deficiency should be considered an important differential diagnosis, particularly in patients with a history of dietary deprivation and incarceration. 

• high-output cardiac failure should prompt investigation of thiamine deficiency as a cause.

Case 1:

72 year-old male with a history of diabetes and remote Whipple procedure who presented with four weeks of weakness and sensory loss. Exam showed distal sensory loss, mild proximal and distal lower limb weakness, and reduced reflexes. Axonal neuropathy was noted on EMG. CSF showed cytoalbuminologic dissociation. IVIG was initiated for a presumptive diagnosis of GBS. He subsequently developed hypotension requiring pressors, lactic acidosis, encephalopathy, ocular muscle weakness and respiratory failure.

Case 2:

38 year-old male with a history of alcoholism and Crohn's was transferred to the facility with 3-4 weeks of progressive sensory and motor deficits, hypotension, tachycardia, and lactic acidosis attributed to GBS and superimposed sepsis. He subsequently developed severe generalized weakness, respiratory failure, encephalopathy and extraocular muscle paresis. Workup revealed axonal neuropathy, no infection and normal CSF findings.

Diagnosis/Treatment:

In both cases, features of Wernicke's and wet beriberi prompted the clinical suspicion supported by brain MRI studies and reduced thiamine levels (19&23 nmol/liter; normal 80-150nmol/liter). Hypotension and cardiac failure rapidly resolved with thiamine repletion. Ocular muscle weakness and encephalopathy resolved within days, but limb weakness only partially improved.

Normal Brain MRI

In conclusion
A high index of suspicion for thiamine deficiency in patients presenting with progressive neuropathy is important as there is significant overlap with GBS. Development of hypotension, tachycardia, lactic acidosis, mental status changes, or extraocular muscle paresis in cases of possible GBS should prompt consideration of thiamine deficiency.