Types of sutures (and when to use them)


There are many types of sutures and they differ by size, material and needle. I made this handy chart to help remember how long each type of material lasts in the body and what it’s commonly used for:

50% Strength Gone Reactivity Use
(coated polyethylene)
indef n/an/a + Tendon
(uncoated polyethylene)
indef n/a + Tendon
Nylon 20%/y n/a + Skin
Silk 1 year >2y ++++ Vessel ligation, drains
indef n/a Skin
Steel indef n/a Tendon, sternum
Fast Gut 6d 20d ++++ Skin
Plain Gut 7d 70d ++++ Skin
Chromic Gut 28d 90d ++++ Oral mucosa
(Poliglecaprone 25)
7d 110d +++ Skin, subcuticular
21d 100d ++ Internal organs, fascia
(Polyglactin 910)
21d 90d ++ Skin, soft tissue

* Monofilament
* Braided

Approach to Primary Amenorrhea


Primary Amenorrhea is defined as the absence of menses:

  • By age 13/14 without normal development of secondary sexual characteristics; OR,
  • By age 15/16, with normal secondary sexual characteristics.

In contrast, Secondary Amenorrhea refers to a loss of menses after it has already been established.

The causes of amenorrea are myriad, with an important one being pregnancy.

Causes of Amenorrhea
Hypothalamus Stress, malnutrition, exercise, lactation, immaturity, Kallmann syndrome
Pituitary Tumor, empty sella, apoplexy, hyperprolactinemia/prolactinoma
Ovaries Gonadal dysgenesis, premature ovarian failure, menopause, ovarian tumor, polycystic ovarian syndrome (PCOS), ovarian enzyme deficiency, chromosomal abnormalities (e.g., 45XO)
Uterus Intrauterine scarring, cervical agenesis, androgen insensitivity
Outflow Tract Imperforate hymen, transverse vaginal septum, cervical stenosis, Mullerian agenesis
Thyroid Hypo/hyperthyroidism
Other Constitutional delay of puberty, hyperandrogenism, Cushing’s syndrome, medications

The most common pathologic causes of Primary Amenorrhea are:

  • Chromosomal abnormalities: 50%
  • Hypothalamic abnormalities: 20%
  • Mullerian agenesis: 5%
  • Pituitary abnormalities: 5%

Determining the etiology of Primary Amenorrhea depends on careful history-taking and a targeted physical exam. Key points to address in the history include:

  • Potential for pregnancy, current lactation
  • Develop of secondary sexual characteristics
    • On a side note, the general order of female sexual development is: breasts, pubic hair, growth spurt, menses; or, “boobs, pubes, grow, flow”
  • Lifestyle factors such as stress, nutrition, exercise, weight changes
  • Medication: THC, antipsychotics, or irradiation
  • Associated symptoms:
    • Hyperprolatinemia: galactorrhea
    • Hyperandrogenism: hair loss/excess, acne, voice change
    • CNS tumor: headaches, visual field deficits, polyuria/polydipsia
    • Family history: Does everyone have relatively late puberty?

In terms of physical exam:

  • Vitals, height, weight
  • Secondary sexual characteristics: breasts, pubic/axillary hair
  • Thyroid: exopthalmos, goiter, abnormal deep tendon reflexes
  • Hyperandrogenism: hirsuitism, acne, hair loss
  • Hypercortisolemia: striae, hyperpigmentation
  • Turner syndrome: webbed neck, low hair line, widely-spaced nipples, short stature
  • Pelvic exam: hymen, vaginal septum, ultrasound for uterine anatomy

Laboratory investigations can offer lots of insight:

  • βHCG: Gotta rule out this common reason first!
  • TSH, PRL: To test for hypo/hyperthyroidism and hyperprolactinemia.
  • LH, FHS: For practicality’s sake, these would probably be ordered at the same time as TSH, PRL.
  • +/- Androgens (testosterone, DHEAS, 17-alpha-hydroxyprogesterone): May indicate PCOS or androgen-secreting tumor, androhen insensitivity syndrome, or 5-alpha-reductase deficiency.
  • +/- Estradiol: These assays lack sensitivity, standardization, and only capture a single time point.

Since chromosomal abnormalities account for half of the pathologic cases of Primary Amenorrhea, karyotyping will be useful for patients who are found to have abnormal uterine anatomy on ultrasound or have elevated FSH, LH. Patients with an absent uterus may be worked-up for abnormal Mullerian development (46XX karyotype and normal female testosterone levels) versus a deficit in masculinization (i.e., androgen insensitivity syndrome, 5-alpha-reductase deficiency). There is a normal uterus, and LH and FSH are high, that means there is nothing feeding back to stop their release; karyotype may reveal Turner syndrome (45XO), while normal karyotype (46XX) may indicate Mullerian agenesis.

The over all treatment goals are to:

  • Treat underlying cause:
    • Lifestyle
    • Discontinue offending medications
    • Surgery
  • Preserve fertility
  • Reduce risk of complications (e.g., remove undescended tests in androgen insensitive patients to mitigate cancer risk).
  • Master-Hunter T, Heiman DL. 2006. Amenorrhea: evaluation and treatment; 73:1374.
  • The Practice Committee of the American Society for Reproductive Medicine. 2008. Current approach to amenorrhea. Fertility and Sterility;90:S219.
  • Welt CK, Barieri RL. Etiology, diagnosis, and treatment of primary amenorrhea. In: UpToDate (Eds: Snyder PJ, Crowley Jr WF, Kirkland JL). Accessed 2013.05.05.

Acute Limb Ischemia

acute limb ischemia

Acute limb ischemia is a sudden decrease in limb perfusion that can potentially threaten limb viability, in patients presenting within 2 weeks of symptom onset (it is considered chronic if more than 2 weeks have passed). The common causes of limb ischemia are:

  • Arterial embolism (80% of cases)
  • Thrombus (usually from site of atherosclerotic plaque)
  • Arterial trauma (e.g., after interventional catheterization procedures)

The symptoms can come on over a period of hours or days. It is important to recognize this condition, in order to improve the chance of limb preservation. Acute limb ischemia is characterized by the 6 P’s:

  • Pain
  • Paresthesia
  • Polar/Poikylothermia (affected extremity is cool on palpation)
  • Pallor
  • Paralysis
  • Pulselessness

If no pulse is palpable, then assessment of perfusion with a Doppler ultrasound is the next step. Note that acutely ischemic limbs may not always appear pale; the extremity may progress to a blue or mottled appearance as the ischemia continues. The most reliable symptoms are paresthesias, which will progress to complete loss of sensation, and paralysis, which may indicate the limb is no longer viable.

Once acute limb ischemia is identified, intravenous heparin is administered. Surgical or endovascular revascularization is the definitive treatment for acute limb ischemia, though these interventions should be performed within 6 hours of symptom onset to improve the probability of limb salvage.

  • Callum K and Bradbury A. 2000. ABC of arterial and venous disease: acute limb ischemia. British Medical Journal; 320:764.
  • Creager MA, Kaufman JA, and Conte MS. 2012. Acute limb ischemia. New England Journal of Medicine; 366:2198.
  • Mitchell ME, Mohler III ER, and Carpenter JP. Acute arterial occlusion of the lower extremities (acute limb ischemia). In: Uptodate (Eds: Clement DL, Hoekstra J, and Collins KA). Accessed 2013.08.24.


Gallbladder Disease (cholelithiasis, biliary colic, cholecystitis, choledocholithiasis, cholangitis)

A lot of the western world have stones in their gallbladders (cholelithiasis) but for the most part they just grumble along with no trouble at all.

  1. Cholelithiasis – Gallstones just hanging out, not causing any problems
  2. Biliary colic – happens after a fatty meal, the GB contracts and pushes stones into the cystic duct but when the duct relaxes the stone rolls back into the GB. The pain is entirely visceral and generally lasts <6h. There should be no fever or chills.
  3. Cholecystitis – inflammation of the GB. It’s biliary colic that just doesn’t go away. The pain lasts longer than 6h and is usually associated with nausea/vomiting, fever and right upper quadrant pain.
  4. Choledocholithiasis – gallstones in the common bile duct. Usually secondary to cholelithiasis, but can be a primary stone in cases of bile stasis or recurrent infection of the biliary tree. Usually have abnormalities in liver enzymes and pain but no fever.
    The 2 major complications are 1) Cholangitis and 2) Acute pancreatitis.
  5. Cholangitis – infection/inflammation of the biliary tree (infected bile or gallstone), secondary to an impacted stone or stricture(s).
    Do an ultrasound. Start antibiotics (common bugs are a mix of gram +/- and anaerobes = E. coli, enterococcus, bactericides). Ciprofloxacin or a combination of ampicillin, ceftazimide and metronidazole.
    Make sure that the person receives some fluid resuscitation to help with the hypoperfusion
    Charcot’s triad: fever, RUQ pain, jaundice
    Reynold’s pentad: hypoperfusion, decreased level of consciousness (SHOCK!!!)

    • Biliary leaks
    • Liver abscess
    • Infected choledochal cysts
    • Cholecystitis
    • Mirizzi syndrome
    • Right lower lobe pneumonia/empyema

Lab values

Biliary Colic Cholecystitis Choledocholithiasis Cholangitis Gallbladder Pancreatitis
WBC  –  ↑ ↑↑  ↑
AST  ↑
Total Bili  – ↑↑ ↑↑
Direct Bili ↑↑ ↑↑↑ ↑↑
ALP ↑↑ ↑↑↑ ↑↑
GGT ↑↑ ↑↑↑ ↑↑
Lipase ↑↑↑ (>3x)
Amylase ↑↑↑ (>3x)
Treatment Cholecystectomy Cholecystectomy ERCP +/- Cholecystectomy Fluid resuscitation ERCP + Cholecystectomy Fluid resuscitation ERCP + Cholecystectomy

Lung surface anatomy and chest tubes vs needle decompression

Surface anatomy of the lungs

  • Lungs extend from about 2 cm above the clavicle down to the 6th rib in the midclavicular line and 8th rib in the midaxillary line
  • The oblique fissure goes from the 6th rib midclavicular line to T3 in the back
  • The horizontal fissure (only on the right) starts at the 4th rib at the sternum and then meets the oblique fissure at the 5th rib in the midaxillary line.
  • The pleura generally is 2 ribs below

Chest Tube

Insert a chest tube in the 4th or 5th intercostal space in the anterior axillary line. When making the incision, make it one rib below the intercostal space you want to insert the tube into. Also, remember to go above the rib, as the neurovascular bundles travel along the underside of the ribs.

These can be done to relieve a pneumothorax, drain a malignant pleural effusion, drain a empyema, or drain a hemopneumothorax. They can also be placed post-operatively following a thoracotomy, esophagectomy or cardiac surgery.

Needle Decompression

These are used in a pinch when a patient is suspected to have a tension pneumothorax and needs immediate decompression. A 14 or 16 gauge needle is inserted above the 2nd or 3rd rib in the midclavicular line.

A tension pneumothorax is recognized by:

  • Dyspnea
  • Hypotension
  • Decreased breath sounds on the affected side
  • Distended neck veins
  • Trachea deviating away from affected side


Blood supply of the GI tract


Turns out there’s a lot of stuff in the abdomen. One could even say there’s almost as much as in the hand. Maybe.

There are three main trunks/arteries off the descending aorta that supply the blood to the guts.

  1. Celiac trunk – foregut (stomach to where the bile duct enters the duodenum)
    1. Common hepatic
      • Hepatic proper
        • Left hepatic
        • Right hepatic
      • Right gastric
      • Gastroduodenal
    2. Left gastric
    3. Splenic
  2. Superior mesenteric artery – midgut (from where the bile duct enters the duodenum to 2/3 across the transverse colon)
    1. Right colic
    2. Middle colic
    3. Ileocolic
    4. Ileal and jejunal branches
  3. Inferior mesenteric artery – hindgut (from 2/3 across the transverse colon to the rectum)
    1. Left colic
    2. Sigmoid
    3. Superior rectal


The stomach is needy and gets a pretty excellent blood supply, which makes remembering is a little tricky

  • Lesser curve: right and left gastric arteries
  • Greater curve: right gastroepipiloic/gastro-omental (off the gastroduodenal artery) and left gastroepipiloic/gastro-omental (off the splenic artery)
  • Fundus: short gastrics (off the splenic artery)

Hemostasis & How to Recognize Bleeding Disorders

Hemostasis – What stops us from bleeding out.

Three main steps:

  1. Vasoconstriction
  2. Primary hemostasis (platelet plug) – the temporary way to stop bleeding
  3. Secondary hemostasis (clotting cascade) – the more permanent way

Bleeding disorders can be broadly divided into whether they affect platelet plug formation or the clotting cascade (if you need a refresher, click here)

 Platelet Disorder Clotting Cascade Disorders
Immediate bleeding
Muscosal and cutaneous
Bruises and petechiae
Nose bleeds (epistaxis)
Menorrhagia (heavy periods)
von Willebrand
Delayed Bleeding
Deep (muscles and joints)
Palpable bruises, large spreading hematomas
Post-surgical bleeding
Hemophilia A (factor VIII)
Hemophilia B (factor IX)

DSM Criteria for Delirium

Delirium, not to be confused with dementia.

The DSM criteria for delirium:

  1. Disturbance of consciousness
  2. Change in cognition
  3. Develops over a short period of time (hours to days) and fluctuates
  4. There is an identifiable general medical condition (or is substance induced)

It is important to recognize a delirium so that the underlying condition can be treated. It is also important because the delirium itself can be harmful to the patient, for example if someone who is delirious walks out into the cold with only a housecoat.

The longer one has delirium, the longer is takes to resolves, even after the underlying condition is treated.

If someone asks you to asses the level of competency of a person with delirium, it’s best to defer. Competency is both TIME- and QUESTION-dependent, so if you are asking someone when they are lucid, they could still be deemed competent, even if they are likely going to return to being delirious.

Mnemonic for delirium: I WATCH DEATH

  1. Infectious: UTIs, pneumonia, meningitis
  2. Withdrawal: alcohol, benzos
  3. Acute metabolic: liver or kidney failure, electrolytes
  4. Trauma: post-op, head injury
  5. CNS pathology: tumor, stroke, seizure
  6. Hypoxia: anemia, PE, heart failure
  7. Deficiencies in vitamins: thiamine, B12, folate
  8. Endocrine: Glucose, thyroid, adrenal, parathyroid (hypercalcemia)
  9. Acute vascular: shock, hypertensive ecephalopathy
  10. Toxins: alcohol, benzos, anticholinergics, opioids, anesthetics, anticonvulsants, dopaminergic agents, steroids, insulin, antibiotics (quinolines), NSAIDs
  11. Heavy metals: lead, arsenic, mercury

Work up


  1. CBC, BUN, Creatinine
  2. Extended electrolytes (Na, K, HCO3, Ca, PO, Mg)
  3. Glucose
  4. Liver function tests
  5. Albumin
  6. Urine culture
  7. TSH
  8. Vitamin B12 & folate

And maybe

  • ECG
  • CXR
  • Blood cultures
  • CT head
  • Heavy metal screen
  • Lumbar puncture
  • EEG

But I want to earn the radiologist tons of money…
Only if they have:

  • Focal neurological deficit
  • Acute change in status
  • Anticoagulant use
  • Acute incontinence
  • Gait abnormality
  • History of cancer

Liver Enzymes (hepatic vs cholestatic patterns)


Liver enzymes can be elevated for a number of reasons, but the first step in an approach is to determine if the enzymes are in a hepatic pattern or cholestatic pattern. It is also very important to realize that Alk phos, GGT, ALP, and AST are liver enzymes, but they don’t give an indication of function; for that you need to look at INR and bilirubin.

Causes of hyponatremia

First – look to see what the person’s sodium is
Second – what is their volume status

The most important thing about hyponatremia is don’t correct more than 8 to 12 mmol/L per day!!!

Also, the paper titled “The Syndrome of Inappropriate Antidiuresis” by Ellison and Berl (N Engl J Med 2007;356:2064-72) is very useful.

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