Severe Acute Malnutrition

Slide 1 · Severe Acute Malnutrition

Wasting, marasmus, kwashiorkor and organ pathology

An integrated clinicopathologic lecture

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Define severe acute malnutrition using the criteria reported.

Distinguish somatic from visceral protein depletion.

Explain the marasmus and kwashiorkor phenotypes mechanistically.

Connect liver, intestinal and marrow lesions to clinical findings.

Slide 3 · Severe wasting is a life-threatening disorder

Severe acute malnutrition is a pediatric wasting syndrome associated with inadequate nutrient intake and/or recurrent illness.

Immune defenses are weakened.

Long-term developmental delays are possible.

Severe wasting increases the risk of death.

Slide 4 · Inadequate intake and illness reinforce each other

Inadequate nutrient intake

Severe nutritional depletion

Impaired immunity

Concurrent infections

Infections add inflammation and metabolic stress, worsening malnutrition.

Slide 5 · Primary versus secondary malnutrition

Primary insufficiency

One or more essential dietary components are missing.

Food supply, poverty and inadequate dietary variety can contribute.

Secondary insufficiency

Intestinal absorption, utilization or storage may fail.

Excess loss or increased metabolic need can create deficits.

Slide 6 · Wasting burden in 2022

45 million

Children under 5 affected by wasting

6.8%

13.6 million

Children under 5 affected by severe wasting

2.1%

These are historical 2022 estimates reported, not updated 2026 surveillance.

Slide 7 · Wasting and stunting are distinct phenomena

Wasting

An acute or recent deficit manifested by low weight relative to height.

Severe wasting is the focus of this lecture.

Stunting

A consequence of malnutrition beginning in utero or early childhood.

Approximately 148 million children under 5 were stunted in 2022 (textbook estimate).

Slide 8 · Severe wasting is concentrated geographically

>75%

Of children with severe wasting live in Asia

2022 estimate

22%

Live in Africa

2022 estimate

The geographic distribution of children with severe wasting.

Slide 9 · Three diagnostic pathways identify severe wasting

MUAC

<115 mm

Weight-for-height

More than 3 SD below normal

Bilateral pitting edema

Lower limbs

The source presents these as alternative criteria for severe acute malnutrition.

Slide 10 · Mid-upper arm circumference: Severe threshold

Mid-upper arm circumference (MUAC) <115 mm

MUAC is a direct anthropometric measurement.

Reduced midarm circumference reflects loss of skeletal-muscle mass.

Interpret in the pediatric assessment context.

Slide 11 · Weight-for-height: Marked deviation from reference

Measured weight

Reference for child’s height

More than 3 SD below normal

This as a severe anthropometric criterion; No unverified cutoffs are added.

Slide 12 · Bilateral pitting edema is a diagnostic clue

Bilateral pitting edema of the lower limbs is a diagnostic criterion.

Examine for fluid accumulation rather than judging by apparent body size.

Edema is especially characteristic of kwashiorkor.

Excess fluid can conceal the underlying tissue loss.

Slide 13 · Weight can conceal depletion when edema is present

Tissue mass decreases

Extracellular fluid accumulates

Observed weight is misleading

Children with kwashiorkor may have substantially more tissue loss than the scale suggests.

Slide 14 · Marasmus and kwashiorkor define a clinical spectrum

MARASMUSSomatic depletion

OVERLAPPING FEATURES

KWASHIORKORVisceral depletion

These endpoints overlap; Individual children may show features of both.

Slide 15 · The two functional protein compartments

Somatic compartment

Proteins in skeletal muscle.

Prominent depletion produces visible muscle wasting.

Visceral compartment

Protein stores in visceral organs, particularly the liver.

Marked depletion is associated with low serum proteins and edema.

Slide 16 · Skinfold thickness reflects subcutaneous fat

Skin

Subcutaneous adipose tissue

Underlying muscle

Reduced thickness in wasting

Skinfold measurement includes skin and subcutaneous tissue; Fat loss reduces the measured thickness.

Slide 17 · Midarm circumference reflects muscle depletion

Muscle

Subcutaneous fat

Skeletal muscle

Circumference decreases when muscle is lost

A smaller midarm circumference can reflect loss of skeletal-muscle protein.

Slide 18 · Serum proteins provide visceral compartment indices

Albumin and transferrin as serum markers.

Their concentrations can help estimate visceral protein status.

They do not replace examination of muscle, fat and edema.

Interpret the laboratory measurements within the overall clinical picture.

Slide 19 · Assessment integrates complementary observations

Observation

What it informs

Weight relative to height

Anthropometric wasting

MUAC / midarm circumference

Somatic muscle depletion

Skinfold thickness

Subcutaneous fat loss

Bilateral pitting edema

Fluid-retaining phenotype

Albumin, transferrin

Visceral protein compartment

Slide 20 · Gut microbiome patterns differ in affected children

Observed association

Children with severe acute malnutrition have microbial flora differing from those of well-nourished children.

Mechanistic uncertainty

A contributory role in pathogenesis is possible.

The source does not establish that a specific bacterial change causes SAM.

Slide 21 · Infection increases the burden of malnutrition

Nutritional depletion

Immune impairment

Secondary infection

Inflammation and catabolism

The infection–malnutrition cycle worsens physiologic reserve.

Slide 22 · Marasmus arises from severe caloric deprivation

Marasmus is the energy-deficient end of the severe malnutrition spectrum.

Severe calorie insufficiency.

Marked loss of fat and muscle is characteristic.

It reports a historical weight criterion of 60% of normal for sex, height and age.

Slide 23 · Marasmus preferentially depletes somatic protein

Calorie deficiency

Muscle protein catabolism

Loss of somatic protein

Severe wasting

Muscle protein is mobilized as part of the adaptive response to energy deficiency.

Slide 24 · Catabolized muscle supplies amino acids

Skeletal muscle proteins

Free amino acids

Metabolic energy needs

This energy-supporting adaptation occurs at the expense of muscle mass.

Slide 25 · Subcutaneous fat becomes an energy source

Energy deficit

Fat mobilization

Subcutaneous fat depletion

Thin extremities

Marasmus produces severe losses of both muscle and subcutaneous fat.

Slide 26 · Leptin and cortisol: A proposed endocrine link

Fat depletion

Lower leptin

Possible HPA activation

Higher cortisol / lipolysis

The leptin–HPA–cortisol sequence as a possible mechanism, not a proven universal pathway.

Slide 27 · Albumin can be relatively preserved in marasmus

Marasmus

Visceral protein compartment is depleted only marginally.

Albumin is often normal or only slightly reduced.

Kwashiorkor

Visceral depletion is severe.

Hypoalbuminemia is associated with edema.

Slide 28 · The marasmic body habitus reflects tissue loss

Extremities are markedly emaciated.

Skeletal-muscle loss is accompanied by subcutaneous fat depletion.

The head appears disproportionately large relative to the wasted body.

Growth retardation accompanies the chronic energy deficit.

Slide 29 · T-cell immunity is impaired in marasmus

Severe undernutrition

Impaired T-cell–mediated immunity

Susceptibility to infection

Intercurrent infection imposes additional stress on a physiologically weakened child.

Slide 30 · Marasmus often has additional deficits

Anemia is a common associated manifestation.

Multiple vitamin deficiencies may coexist.

Cell-mediated immunodeficiency increases infectious complications.

A marasmic phenotype does not mean isolated calorie deficiency without other deficits.

Slide 31 · Kwashiorkor reflects disproportionate protein lack

Protein deprivation is relatively greater than the fall in total calories.

Visceral protein is markedly depleted.

Fluid retention produces the characteristic edema.

The two classical phenotypes are endpoints, not separate sealed categories.

Slide 32 · Dietary transitions can contribute to kwashiorkor

Early weaning

Predominantly carbohydrate diet

Relative protein deprivation

Kwashiorkor phenotype

This feeding pattern is the textbook’s classic setting; It is not the only etiologic pathway.

Slide 33 · Protein loss and malabsorption create other settings

Clinical context

Mechanism identified in Robbins

Chronic diarrheal states

Impaired protein absorption

Protein-losing enteropathy

Gastrointestinal protein loss

Nephrotic syndrome

Renal protein loss

Extensive burns

Loss of body protein

Restrictive / unusual diets

Marked dietary protein inadequacy

Slide 34 · Visceral protein depletion is central in kwashiorkor

Marked dietary protein lack

Visceral protein depletion

Low serum albumin

Edema

The pathophysiology directly links a visceral-compartment deficit to the edematous phenotype.

Slide 35 · Hypoalbuminemia accompanies fluid accumulation

Intravascular compartment

Albumin decreases

Edema

Generalized / dependent fluid accumulation

Generalized or dependent edema can be prominent, including facial and limb puffiness and ascites.

Slide 36 · Retained fluid masks the extent of tissue loss

A child with severe kwashiorkor may appear heavier because of edema.

Historical weights of 60%–80% of normal.

Observed weight can overestimate remaining tissue mass.

Examination must account for edema when interpreting nutritional status.

Slide 37 · Muscle and fat may seem less reduced in kwashiorkor

Relative preservation

Compared with marasmus, muscle and subcutaneous fat are less depleted.

Important caveat

Edema can also mask losses in these compartments.

Relative sparing does not mean normal tissue reserves.

Slide 38 · Kwashiorkor dermatosis has a “flaky paint” pattern

Hyperpigmentation

Desquamation

Hypopigmentation

Schematic of descriptive features — not a clinical photograph

Alternating hyperpigmentation, desquamation and hypopigmentation form the characteristic described appearance.

Slide 39 · Kwashiorkor changes hair texture and pigmentation

Feature

Textbook description

Pigmentation

Loss of color or alternating pale and dark bands

Architecture

Hair may straighten and become fine

Attachment

Hair is less firmly attached to the scalp

Slide 40 · The enlarged fatty liver is diagnostically useful

Reduced carrier protein components

Impaired lipoprotein transport

Fat accumulation in liver

Hepatomegaly

Fatty hepatomegaly in kwashiorkor, in contrast to marasmus.

Slide 41 · Apathy and poor appetite distinguish kwashiorkor

Apathy and listlessness are characteristic clinical changes.

Loss of appetite may accompany the visceral protein deficit.

Edema, dermatosis, hair changes and fatty liver strengthen the pattern.

Slide 42 · Both phenotypes share nutritional and immune harm

Marasmus

Anemia and multiple vitamin deficiencies.

Defects in cell-mediated immunity.

Concurrent infection may be present.

Kwashiorkor

Associated vitamin deficiencies.

Immune defects and secondary infection.

Infection-driven catabolism worsens the state.

Slide 43 · Marasmus and kwashiorkor compared

Feature

Marasmus

Kwashiorkor

Dominant deficit

Total calories

Protein disproportionate

Protein store

Somatic / muscle

Visceral / liver

Subcutaneous fat

Markedly lost

Relatively spared

Albumin

Normal / mildly low

Markedly decreased

Edema

Not a defining feature

Prominent

Liver

Usually not fatty

Fatty, often enlarged

Skin / hair

No classic pattern specified

Flaky paint; color / texture changes

Slide 44 · Three principal anatomic findings in severe malnutrition

Growth

Growth failure

Fluid

Peripheral edema: Kwashiorkor

Tissue

Fat loss + muscle atrophy

The relative prominence of these findings varies by phenotype.

Slide 45 · The liver is fatty in kwashiorkor, not marasmus

Kwashiorkor

Enlarged, fatty liver is characteristic.

Superimposed cirrhosis is rare.

Marasmus

Fatty hepatomegaly is not characteristic in the cited morphologic description.

Marked peripheral fat and muscle loss predominate.

Slide 46 · Intestinal crypt proliferation may fall

Kwashiorkor

Fewer mitotic crypt cells

Reduced mucosal renewal

Mucosal atrophy

This crypt abnormality is described in kwashiorkor, rarely in marasmus.

Slide 47 · Small bowel villi and microvilli may atrophy

Reference mucosa

Kwashiorkor-associated atrophy

Schematic only: Relative villous height is illustrative; Microvilli are not drawn

Slide 48 · Disaccharidase deficiency follows mucosal injury

Mucosal atrophy

Loss of small-intestinal enzymes

Disaccharidase deficiency

Poor initial milk tolerance

Full-strength milk-based diets may initially be poorly tolerated.

Slide 49 · Intestinal mucosal changes can reverse

The intestinal mucosal changes described in kwashiorkor are reversible with treatment.

Crypt cell activity and mucosal structure can recover.

Enzyme depletion helps explain temporary feeding intolerance.

This slide reports pathology and does not prescribe a treatment protocol.

Slide 50 · Bone marrow may become hypoplastic

Severe nutritional deficit

Reduced erythroid precursors

Hypoplastic bone marrow

Anemia

The marrow change is reported in both marasmus and kwashiorkor.

Slide 51 · Anemia has overlapping etiologies

Iron / folate / protein deficits

Infectious inflammation

Reduced erythropoiesis

Anemia

Robbins characterizes the anemia as usually mild to moderate and multifactorial.

Slide 52 · Red-cell size depends on the dominant factor

Microcytic

Normocytic

Macrocytic

Microcytic, normocytic or macrocytic anemia may occur; Size alone does not identify the nutritional syndrome.

Schematic: Not peripheral blood-smear imagery

Slide 53 · Read organ morphology as a connected process

Site

Lesion

Clinicopathologic implication

Skeletal muscle

Atrophy / catabolism

Visible wasting

Liver

Steatosis in kwashiorkor

Enlargement

Small bowel

Villus/microvillus loss

Disaccharidase deficiency

Bone marrow

Reduced red-cell precursors

Anemia

Extracellular space

Edema in kwashiorkor

Apparent mass can be misleading

Slide 54 · Case: Severe wasting without edema

A young child has strikingly thin limbs, very little subcutaneous fat, growth failure, and no prominent edema. Albumin is not markedly reduced.

Which protein compartment is most depleted, and which phenotype predominates?

Slide 55 · Case interpretation: Marasmus-predominant

Somatic (skeletal-muscle) protein loss predominates.

Energy deficiency mobilizes muscle protein and adipose stores.

Visceral proteins may be relatively preserved.

The phenotype is marasmus-predominant.

Slide 56 · Case: Edema, hair change and enlarged liver

A child has bilateral pitting edema, facial puffiness, sparse pale hair, skin desquamation and hepatomegaly despite a less strikingly low apparent weight.

What explains the edema, and which phenotype is most likely?

Slide 57 · Case interpretation: Kwashiorkor-predominant

Visceral protein loss with hypoalbuminemia explains the edema.

Fluid retention masks actual tissue depletion.

Fatty liver, dermatosis and hair changes support kwashiorkor.

Clinical syndromes can still overlap.

Slide 58 · Pathogenesis connects to the characteristic lesions

Mechanism

Principal lesion or sign

Somatic protein catabolism

Skeletal-muscle atrophy

Fat mobilization

Decreased subcutaneous fat

Visceral protein depletion

Low albumin, edema

Lipoprotein-component deficit

Hepatic steatosis

Reduced intestinal crypt renewal

Mucosal atrophy / enzyme loss

Reduced erythroid precursors

Anemia

Slide 59 · Primary references and scope

Robbins, Cotran & Kumar. Pathologic Basis of Disease. 11th ed. Environmental and Nutritional Diseases (nutritional disorders section).

Chapter sections: Dietary Insufficiency; Severe Acute Malnutrition; Marasmus; Kwashiorkor; Morphology.

Burden estimates correspond to 2022 data quoted by the textbook; no external updates or treatment protocols have been inserted.